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Current Pharmaceutical Design

Editor-in-Chief

ISSN (Print): 1381-6128
ISSN (Online): 1873-4286

Review Article

Potential Protein Blood-based Biomarkers in Different Types of Dementia: A Therapeutic Overview

Author(s): Patricia R. Manzine*, Izabela P. Vatanabe, Marina M. Grigoli, Renata V. Pedroso, Maria Patricia A.O. Monteiro, Danielle S.M.S. Oliveira, Carla M.C. Nascimento, Rafaela Peron, Fabiana S. Orlandi and Márcia R. Cominetti

Volume 28, Issue 14, 2022

Published on: 31 May, 2022

Page: [1170 - 1186] Pages: 17

DOI: 10.2174/1381612828666220408124809

Price: $65

Abstract

Biomarkers capable of identifying and distinguishing types of dementia, such as Alzheimer's disease (AD), Parkinson's disease dementia (PDD), Lewy body dementia (LBD), and frontotemporal dementia (FTD), have become increasingly relentless. Studies on possible biomarker proteins in the blood that can help formulate new diagnostic proposals and therapeutic visions of different types of dementia are needed. However, due to several limitations of these biomarkers, especially in discerning dementia, their clinical applications are still undetermined. Thus, updating biomarker blood proteins that can help in the diagnosis and discrimination of these main dementia conditions is essential to enable new pharmacological and clinical management strategies with specificities for each type of dementia. This paper aimed to review the literature concerning protein bloodbased AD and non-AD biomarkers as new pharmacological targets and/or therapeutic strategies. Recent findings related to protein-based AD, PDD, LBD, and FTD biomarkers are focused on in this review. Protein biomarkers are classified according to the pathophysiology of the dementia types. The diagnosis and distinction of dementia through protein biomarkers is still a challenge. The lack of exclusive biomarkers for each type of dementia highlights the need for further studies in this field. Only after this, blood biomarkers may have a valid use in clinical practice as they are promising to help in the diagnosis and in the differentiation of diseases.

Keywords: Blood, biomarkers, diagnosis, treatments, elderly, dementia.

[1]
Forester BP, Gatchel JR. Medical co-morbidity, brain disease, and the future of geriatric psychiatry. Am J Geriatr Psychiatry 2014; 22(11): 1061-5.
[http://dx.doi.org/10.1016/j.jagp.2014.08.007] [PMID: 25307312]
[2]
Kovacs GG. Molecular pathological classification of neurodegenerative diseases: Turning towards precision medicine. Int J Mol Sci 2016; 17(2): E189.
[http://dx.doi.org/10.3390/ijms17020189] [PMID: 26848654]
[3]
Dodge HH, Zhu J, Woltjer R, et al. Risk of incident clinical diagnosis of Alzheimer’s disease-type dementia attributable to pathology-confirmed vascular disease. Alzheimer’s Dement 2017; 13(6): 613-23.
[http://dx.doi.org/10.1016/j.jalz.2016.11.003] [PMID: 28017827]
[4]
Sperling R, Mormino E, Johnson K. The evolution of preclinical Alzheimer’s disease: Implications for prevention trials. Neuron 2014; 84(3): 608-22.
[http://dx.doi.org/10.1016/j.neuron.2014.10.038] [PMID: 25442939]
[5]
Ashton NJ, Hye A, Rajkumar AP, et al. An update on blood-based biomarkers for non-Alzheimer neurodegenerative disorders. Nat Rev Neurol 2020; 16(5): 265-84.
[http://dx.doi.org/10.1038/s41582-020-0348-0] [PMID: 32322100]
[6]
Molinuevo JL, Ayton S, Batrla R, et al. Current state of Alzheimer’s fluid biomarkers. Acta Neuropathol 2018; 136(6): 821-53.
[http://dx.doi.org/10.1007/s00401-018-1932-x] [PMID: 30488277]
[7]
O’Bryant SE, Mielke MM, Rissman RA, et al. Blood-based biomarkers in Alzheimer disease: Current state of the science and a novel collaborative paradigm for advancing from discovery to clinic. Alzheimer’s Dement 2017; 13(1): 45-58.
[http://dx.doi.org/10.1016/j.jalz.2016.09.014] [PMID: 27870940]
[8]
O’Bryant SE, Gupta V, Henriksen K, et al. Guidelines for the standardization of preanalytic variables for blood-based biomarker studies in Alzheimer’s disease research. Alzheimer’s Dement 2015; 11(5): 549-60.
[http://dx.doi.org/10.1016/j.jalz.2014.08.099] [PMID: 25282381]
[9]
Karikari TK, Pascoal TA, Ashton NJ, et al. Blood phosphorylated tau 181 as a biomarker for Alzheimer’s disease: A diagnostic performance and prediction modelling study using data from four prospective cohorts. Lancet Neurol 2020; 19(5): 422-33.
[http://dx.doi.org/10.1016/S1474-4422(20)30071-5] [PMID: 32333900]
[10]
Oliveira Monteiro MPA, Salheb Oliveira DSM, Manzine PR, et al. ADAM10 plasma levels predict worsening in cognition of older adults: A 3-year follow-up study. Alzheimer’s Res Ther 2021; 13(1): 18.
[http://dx.doi.org/10.1186/s13195-020-00750-y] [PMID: 33419480]
[11]
Hampel H, O’Bryant SE, Molinuevo JL, et al. Blood-based biomarkers for Alzheimer disease: Mapping the road to the clinic. Nat Rev Neurol 2018; 14(11): 639-52.
[http://dx.doi.org/10.1038/s41582-018-0079-7] [PMID: 30297701]
[12]
Zetterberg H, Burnham SC. Blood-based molecular biomarkers for Alzheimer’s disease. Mol Brain 2019; 12(1): 26.
[http://dx.doi.org/10.1186/s13041-019-0448-1] [PMID: 30922367]
[13]
Henriksen K, O’Bryant SE, Hampel H, et al. The future of blood-based biomarkers for Alzheimer’s disease. Alzheimer’s Dement 2014; 10(1): 115-31.
[http://dx.doi.org/10.1016/j.jalz.2013.01.013] [PMID: 23850333]
[14]
Blennow K, Hampel H, Zetterberg H. Biomarkers in amyloid-β immunotherapy trials in Alzheimer’s disease. Neuropsychopharmacology 2014; 39(1): 189-201.
[http://dx.doi.org/10.1038/npp.2013.154] [PMID: 23799530]
[15]
Long JM, Ray B, Lahiri DK. MicroRNA-339-5p down-regulates protein expression of β-site amyloid precursor protein-cleaving enzyme 1 (BACE1) in human primary brain cultures and is reduced in brain tissue specimens of Alzheimer disease subjects. J Biol Chem 2014; 289(8): 5184-98.
[http://dx.doi.org/10.1074/jbc.M113.518241] [PMID: 24352696]
[16]
Shen Y, Wang H, Sun Q, et al. Increased plasma beta-secretase 1 may predict conversion to Alzheimer’s disease dementia in individuals with mild cognitive impairment. Biol Psychiatry 2018; 83(5): 447-55.
[http://dx.doi.org/10.1016/j.biopsych.2017.02.007] [PMID: 28359566]
[17]
Akhter R, Shao Y, Shaw M, et al. Regulation of ADAM10 by miR-140-5p and potential relevance for Alzheimer’s disease. Neurobiol Aging 2018; 63: 110-9.
[http://dx.doi.org/10.1016/j.neurobiolaging.2017.11.007] [PMID: 29253717]
[18]
Huang WH, Chen W, Jiang LY, Yang YX, Yao LF, Li KS. Influence of ADAM10 polymorphisms on plasma level of soluble receptor for advanced glycation end products and the association with Alzheimer’s disease risk. Front Genet 2018; 9: 540.
[http://dx.doi.org/10.3389/fgene.2018.00540] [PMID: 30555509]
[19]
Manzine PR, Barham EJ, Vale FA, Selistre-de-Araújo HS, Pavarini SC, Cominetti MR. Platelet a disintegrin and metallopeptidase 10 expression correlates with clock drawing test scores in Alzheimer’s disease. Int J Geriatr Psychiatry 2014; 29(4): 414-20.
[http://dx.doi.org/10.1002/gps.4020] [PMID: 23970375]
[20]
Manzine PR, Barham EJ, Vale FA, Selistre-de-Araújo HS, Iost Pavarini SC, Cominetti MR. Correlation between mini-mental state examination and platelet ADAM10 expression in Alzheimer’s disease. J Alzheimer’s Dis 2013; 36(2): 253-60.
[http://dx.doi.org/10.3233/JAD-130125] [PMID: 23579328]
[21]
Manzine PR, Vatanabe IP, Peron R, et al. Blood-based Biomarkers of Alzheimer’s Disease: The Long and Winding Road. Curr Pharm Des 2020; 26(12): 1300-15.
[http://dx.doi.org/10.2174/1381612826666200114105515] [PMID: 31942855]
[22]
Nakamura A, Kaneko N, Villemagne VL, et al. High performance plasma amyloid-β biomarkers for Alzheimer’s disease. Nature 2018; 554(7691): 249-54.
[http://dx.doi.org/10.1038/nature25456] [PMID: 29420472]
[23]
Janelidze S, Stomrud E, Palmqvist S, et al. Plasma β-amyloid in Alzheimer’s disease and vascular disease. Sci Rep 2016; 6(1): 26801.
[http://dx.doi.org/10.1038/srep26801] [PMID: 27241045]
[24]
Schindler SE, Bollinger JG, Ovod V, et al. High-precision plasma β-amyloid 42/40 predicts current and future brain amyloidosis. Neurology 2019; 93(17): e1647-59.
[http://dx.doi.org/10.1212/WNL.0000000000008081] [PMID: 31371569]
[25]
Palmqvist S, Janelidze S, Stomrud E, et al. Performance of fully automated plasma assays as screening tests for Alzheimer Disease-related β-amyloid status. JAMA Neurol 2019; 76(9): 1060-9.
[http://dx.doi.org/10.1001/jamaneurol.2019.1632] [PMID: 31233127]
[26]
Mattsson N, Zetterberg H, Janelidze S, et al. Plasma tau in Alzheimer disease. Neurology 2016; 87(17): 1827-35.
[http://dx.doi.org/10.1212/WNL.0000000000003246] [PMID: 27694257]
[27]
Mielke MM, Hagen CE, Xu J, et al. Plasma phospho-tau181 increases with Alzheimer’s disease clinical severity and is associated with tau- and amyloid-positron emission tomography. Alzheimer’s Dement 2018; 14(8): 989-97.
[http://dx.doi.org/10.1016/j.jalz.2018.02.013] [PMID: 29626426]
[28]
Thijssen EH, La Joie R, Wolf A, et al. Diagnostic value of plasma phosphorylated tau181 in Alzheimer’s disease and frontotemporal lobar degeneration. Nat Med 2020; 26(3): 387-97.
[http://dx.doi.org/10.1038/s41591-020-0762-2] [PMID: 32123386]
[29]
Janelidze S, Mattsson N, Palmqvist S, et al. Plasma P-tau181 in Alzheimer’s disease: Relationship to other biomarkers, differential diagnosis, neuropathology and longitudinal progression to Alzheimer’s dementia. Nat Med 2020; 26(3): 379-86.
[http://dx.doi.org/10.1038/s41591-020-0755-1] [PMID: 32123385]
[30]
Suárez-Calvet M, Karikari TK, Ashton NJ, et al. Novel tau biomarkers phosphorylated at T181, T217 or T231 rise in the initial stages of the preclinical Alzheimer’s continuum when only subtle changes in Aβ pathology are detected. EMBO Mol Med 2020; 12(12): e12921.
[http://dx.doi.org/10.15252/emmm.202012921] [PMID: 33169916]
[31]
Hall S, Janelidze S, Londos E, et al. Plasma phospho-tau identifies Alzheimer’s co-pathology in patients with lewy body disease. Mov Disord 2021; 36(3): 767-71.
[http://dx.doi.org/10.1002/mds.28370] [PMID: 33285015]
[32]
Ashton NJ, Pascoal TA, Karikari TK, et al. Plasma p-tau231: A new biomarker for incipient Alzheimer’s disease pathology. Acta Neuropathol 2021; 141(5): 709-24.
[http://dx.doi.org/10.1007/s00401-021-02275-6] [PMID: 33585983]
[33]
Mattsson N, Andreasson U, Zetterberg H, Blennow K. Association of plasma neurofilament light with neurodegeneration in patients with Alzheimer disease. JAMA Neurol 2017; 74(5): 557-66.
[http://dx.doi.org/10.1001/jamaneurol.2016.6117] [PMID: 28346578]
[34]
Mattsson N, Cullen NC, Andreasson U, Zetterberg H, Blennow K. Association between longitudinal plasma neurofilament light and neurodegeneration in patients With Alzheimer disease. JAMA Neurol 2019; 76(7): 791-9.
[http://dx.doi.org/10.1001/jamaneurol.2019.0765] [PMID: 31009028]
[35]
Preische O, Schultz SA, Apel A, et al. Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease. Nat Med 2019; 25(2): 277-83.
[http://dx.doi.org/10.1038/s41591-018-0304-3] [PMID: 30664784]
[36]
Blasko I, Jellinger K, Kemmler G, et al. Conversion from cognitive health to mild cognitive impairment and Alzheimer’s disease: Prediction by plasma amyloid beta 42, medial temporal lobe atrophy and homocysteine. Neurobiol Aging 2008; 29(1): 1-11.
[http://dx.doi.org/10.1016/j.neurobiolaging.2006.09.002] [PMID: 17055615]
[37]
Graff-Radford NRC, Crook JE, Lucas J, et al. Association of low plasma Abeta42/Abeta40 ratios with increased imminent risk for mild cognitive impairment and Alzheimer disease. Arch Neurol 2007; 64(3): 354-62.
[http://dx.doi.org/10.1001/archneur.64.3.354] [PMID: 17353377]
[38]
Blennow K, Hampel H, Weiner M, Zetterberg H. Cerebrospinal fluid and plasma biomarkers in Alzheimer disease. Nat Rev Neurol 2010; 6(3): 131-44.
[http://dx.doi.org/10.1038/nrneurol.2010.4] [PMID: 20157306]
[39]
Mukaetova-Ladinska E, Abdell-All Z, Andrade J, et al. Platelet tau protein as a potential peripheral biomarker in Alzheimer’s disease: An explorative study 2018; 15(9): 800-8.
[40]
Park JC, Han SH, Yi D, et al. Plasma tau/amyloid-β1-42 ratio predicts brain tau deposition and neurodegeneration in Alzheimer’s disease. Brain 2019; 142(3): 771-86.
[http://dx.doi.org/10.1093/brain/awy347] [PMID: 30668647]
[41]
Chen Z, Mengel D, Keshavan A, et al. Learnings about the complexity of extracellular tau aid development of a blood-based screen for Alzheimer’s disease. Alzheimer’s Dement 2019; 15(3): 487-96.
[http://dx.doi.org/10.1016/j.jalz.2018.09.010] [PMID: 30419228]
[42]
Nabers A, Perna L, Lange J, et al. Amyloid blood biomarker detects Alzheimer’s disease. EMBO Mol Med 2018; 10(5): e8763.
[http://dx.doi.org/10.15252/emmm.201708763] [PMID: 29626112]
[43]
Nabers A, Hafermann H, Wiltfang J, Gerwert K. Aβ and tau structure-based biomarkers for a blood- and CSF-based two-step recruitment strategy to identify patients with dementia due to Alzheimer’s disease. Alzheimer’s Dement (Amst) 2019; 11(1): 257-63.
[http://dx.doi.org/10.1016/j.dadm.2019.01.008] [PMID: 30911600]
[44]
Lane CA, Hardy J, Schott JM. Alzheimer’s disease. Eur J Neurol 2018; 25(1): 59-70.
[http://dx.doi.org/10.1111/ene.13439] [PMID: 28872215]
[45]
Slachevsky A, Guzmán-Martínez L, Delgado C, et al. Tau platelets correlate with regional brain atrophy in patients with Alzheimer’s disease. J Alzheimer’s Dis 2017; 55(4): 1595-603.
[http://dx.doi.org/10.3233/JAD-160652] [PMID: 27911301]
[46]
Guzmán-Martínez L, Tapia JP, Farías GA, González A, Estrella M, Maccioni RB. The alz-tau biomarker for Alzheimer’s disease: Study in a caucasian population. J Alzheimer’s Dis 2019; 67(4): 1181-6.
[http://dx.doi.org/10.3233/JAD-180637] [PMID: 30775977]
[47]
Giunta B, Fernandez F, Nikolic WV, et al. Inflammaging as a prodrome to Alzheimer’s disease. J Neuroinflammation 2008; 5(1): 51.
[http://dx.doi.org/10.1186/1742-2094-5-51] [PMID: 19014446]
[48]
Popp J, Oikonomidi A, Tautvydaitė D, et al. Markers of neuroinflammation associated with Alzheimer’s disease pathology in older adults. Brain Behav Immun 2017; 62: 203-11.
[http://dx.doi.org/10.1016/j.bbi.2017.01.020] [PMID: 28161476]
[49]
Neher JJ, Cunningham C. Priming microglia for innate immune memory in the brain. Trends Immunol 2019; 40(4): 358-74.
[http://dx.doi.org/10.1016/j.it.2019.02.001] [PMID: 30833177]
[50]
Okello A, Edison P, Archer HA, et al. Microglial activation and amyloid deposition in mild cognitive impairment: A PET study. Neurology 2009; 72(1): 56-62.
[http://dx.doi.org/10.1212/01.wnl.0000338622.27876.0d] [PMID: 19122031]
[51]
Magaki S, Mueller C, Dickson C, Kirsch W. Increased production of inflammatory cytokines in mild cognitive impairment. Exp Gerontol 2007; 42(3): 233-40.
[http://dx.doi.org/10.1016/j.exger.2006.09.015] [PMID: 17085001]
[52]
Tejera D, Heneka MT. Microglia in Alzheimer’s disease: The good, the bad and the ugly. Curr Alzheimer Res 2016; 13(4): 370-80.
[http://dx.doi.org/10.2174/1567205013666151116125012] [PMID: 26567746]
[53]
Trollor JN, Smith E, Agars E, et al. The association between systemic inflammation and cognitive performance in the elderly: The Sydney memory and ageing study. Age 2012; 34(5): 1295-308.
[http://dx.doi.org/10.1007/s11357-011-9301-x] [PMID: 21853262]
[54]
Macy EM, Hayes TE, Tracy RP. Variability in the measurement of C-reactive protein in healthy subjects: Implications for reference intervals and epidemiological applications. Clin Chem 1997; 43(1): 52-8.
[http://dx.doi.org/10.1093/clinchem/43.1.52] [PMID: 8990222]
[55]
Hilal S, Ikram MA, Verbeek MM, et al. C-Reactive protein, plasma amyloid-β levels, and their interaction with magnetic resonance imaging markers. Stroke 2018; 49(11): 2692-8.
[http://dx.doi.org/10.1161/STROKEAHA.118.022317] [PMID: 30355213]
[56]
Uslu S, Akarkarasu ZE, Ozbabalik D, et al. Levels of amyloid beta-42, interleukin-6 and tumor necrosis factor-alpha in Alzheimer’s disease and vascular dementia. Neurochem Res 2012; 37(7): 1554-9.
[http://dx.doi.org/10.1007/s11064-012-0750-0] [PMID: 22437436]
[57]
Zuliani G, Ranzini M, Guerra G, et al. Plasma cytokines profile in older subjects with late onset Alzheimer’s disease or vascular dementia. J Psychiatr Res 2007; 41(8): 686-93.
[http://dx.doi.org/10.1016/j.jpsychires.2006.02.008] [PMID: 16600299]
[58]
Brosseron F, Krauthausen M, Kummer M, Heneka MT. Body fluid cytokine levels in mild cognitive impairment and Alzheimer’s disease: A comparative overview. Mol Neurobiol 2014; 50(2): 534-44.
[http://dx.doi.org/10.1007/s12035-014-8657-1] [PMID: 24567119]
[59]
Kreuzer KA, Rockstroh JK, Sauerbruch T, Spengler U. A comparative study of different enzyme immunosorbent assays for human tumor necrosis factor-alpha. J Immunol Methods 1996; 195(1-2): 49-54.
[http://dx.doi.org/10.1016/0022-1759(96)00090-7] [PMID: 8814319]
[60]
Wajant H, Pfizenmaier K, Scheurich P. Tumor necrosis factor signaling. Cell Death Differ 2003; 10(1): 45-65.
[http://dx.doi.org/10.1038/sj.cdd.4401189] [PMID: 12655295]
[61]
Buchhave P, Zetterberg H, Blennow K, Minthon L, Janciauskiene S, Hansson O. Soluble TNF receptors are associated with Aβ metabolism and conversion to dementia in subjects with mild cognitive impairment. Neurobiol Aging 2010; 31(11): 1877-84.
[http://dx.doi.org/10.1016/j.neurobiolaging.2008.10.012] [PMID: 19070941]
[62]
Decourt B, Lahiri DK, Sabbagh MN. Targeting tumor necrosis factor alpha for Alzheimer’s disease. Curr Alzheimer Res 2017; 14(4): 412-25.
[http://dx.doi.org/10.2174/1567205013666160930110551] [PMID: 27697064]
[63]
Monson NL, Ireland SJ, Ligocki AJ, et al. Elevated CNS inflammation in patients with preclinical Alzheimer’s disease. J Cereb Blood Flow Metab 2014; 34(1): 30-3.
[http://dx.doi.org/10.1038/jcbfm.2013.183] [PMID: 24149932]
[64]
Gupta PP, Pandey RD, Jha D, Shrivastav V, Kumar S. Role of traditional nonsteroidal anti-inflammatory drugs in Alzheimer’s disease: A meta-analysis of randomized clinical trials. Am J Alzheimer’s Dis Other Demen 2015; 30(2): 178-82.
[http://dx.doi.org/10.1177/1533317514542644] [PMID: 25024454]
[65]
Aisen PS. The potential of anti-inflammatory drugs for the treatment of Alzheimer’s disease. Lancet Neurol 2002; 1(5): 279-84.
[http://dx.doi.org/10.1016/S1474-4422(02)00133-3] [PMID: 12849425]
[66]
Cheng Z, Yin J, Yuan H, et al. Blood-derived plasma protein biomarkers for Alzheimer’s disease in Han Chinese. Front Aging Neurosci 2018; 10: 414.
[http://dx.doi.org/10.3389/fnagi.2018.00414] [PMID: 30618720]
[67]
McLimans KE, Webb JL, Anantharam V, Kanthasamy A, Willette AA. Peripheral versus central index of metabolic dysfunction and associations with clinical and pathological outcomes in Alzheimer’s disease. J Alzheimer’s Dis 2017; 60(4): 1313-24.
[http://dx.doi.org/10.3233/JAD-170263] [PMID: 28968233]
[68]
Schindler N, Mayer J, Saenger S, et al. Phenotype analysis of male transgenic mice overexpressing mutant IGFBP-2 lacking the Cardin-Weintraub sequence motif: Reduced expression of synaptic markers and myelin basic protein in the brain and a lower degree of anxiety-like behaviour. Growth Horm IGF Res 2017; 33: 1-8.
[http://dx.doi.org/10.1016/j.ghir.2016.11.003] [PMID: 27919008]
[69]
Bennett S, Grant M, Creese AJ, et al. Plasma levels of complement 4a protein are increased in Alzheimer’s disease. Alzheimer Dis Assoc Disord 2012; 26(4): 329-34.
[http://dx.doi.org/10.1097/WAD.0b013e318239dcbd] [PMID: 22052466]
[70]
Uchida K, Shan L, Suzuki H, et al. Amyloid-β sequester proteins as blood-based biomarkers of cognitive decline. Alzheimer’s Dement (Amst) 2015; 1(2): 270-80.
[http://dx.doi.org/10.1016/j.dadm.2015.04.003] [PMID: 27239510]
[71]
Petzold A. Neurofilament phosphoforms: Surrogate markers for axonal injury, degeneration and loss. J Neurol Sci 2005; 233(1-2): 183-98.
[http://dx.doi.org/10.1016/j.jns.2005.03.015] [PMID: 15896809]
[72]
Lewczuk P, Ermann N, Andreasson U, et al. Plasma neurofilament light as a potential biomarker of neurodegeneration in Alzheimer’s disease. Alzheimer’s Res Ther 2018; 10(1): 71.
[http://dx.doi.org/10.1186/s13195-018-0404-9] [PMID: 30055655]
[73]
Blennow K. A review of fluid biomarkers for Alzheimer’s disease: Moving from CSF to blood. Neurol Ther 2017; 6(S1)(Suppl. 1): 15-24.
[http://dx.doi.org/10.1007/s40120-017-0073-9] [PMID: 28733960]
[74]
Weston PSJ, Poole T, Ryan NS, et al. Serum neurofilament light in familial Alzheimer disease: A marker of early neurodegeneration. Neurology 2017; 89(21): 2167-75.
[http://dx.doi.org/10.1212/WNL.0000000000004667] [PMID: 29070659]
[75]
Yao F, Zhang K, Zhang Y, et al. Identification of blood biomarkers for Alzheimer’s disease through computational prediction and experimental validation. Front Neurol 2019; 9: 1158.
[http://dx.doi.org/10.3389/fneur.2018.01158] [PMID: 30671019]
[76]
Mroczko B, Groblewska M, Zboch M, et al. Concentrations of matrix metalloproteinases and their tissue inhibitors in the cerebrospinal fluid of patients with Alzheimer’s disease. J Alzheimer’s Dis 2014; 40(2): 351-7.
[http://dx.doi.org/10.3233/JAD-131634] [PMID: 24448781]
[77]
Hernández-Guillamon M, Delgado P, Ortega L, et al. Neuronal TIMP-1 release accompanies astrocytic MMP-9 secretion and enhances astrocyte proliferation induced by beta-amyloid 25-35 fragment. J Neurosci Res 2009; 87(9): 2115-25.
[http://dx.doi.org/10.1002/jnr.22034] [PMID: 19235898]
[78]
Martínez-Morillo E, Hansson O, Atagi Y, et al. Total apolipoprotein E levels and specific isoform composition in cerebrospinal fluid and plasma from Alzheimer’s disease patients and controls. 2014; 127(5): 633-43.
[http://dx.doi.org/10.1007/s00401-014-1266-2]
[79]
Rasmussen KL, Tybjaerg-Hansen A, Nordestgaard BG, et al. Plasma apolipoprotein E levels and risk of dementia: A Mendelian randomization study of 106,562 individuals 2018; 14(1): 71-80.
[80]
Safieh M, Korczyn AD, Michaelson DM. ApoE4: An emerging therapeutic target for Alzheimer’s disease. BMC Med 2019; 17(1): 64.
[http://dx.doi.org/10.1186/s12916-019-1299-4] [PMID: 30890171]
[81]
Weinstein G, Beiser AS, Preis SR, et al. Plasma clusterin levels and risk of dementia, Alzheimer’s disease, and stroke. Alzheimer’s Dement (Amst) 2016; 3(1): 103-9.
[http://dx.doi.org/10.1016/j.dadm.2016.06.005] [PMID: 27453932]
[82]
Gupta VB, Hone E, Pedrini S, et al. Altered levels of blood proteins in Alzheimer’s disease longitudinal study: Results from Australian imaging biomarkers lifestyle study of ageing cohort. Alzheimer’s Dement (Amst) 2017; 8(1): 60-72.
[http://dx.doi.org/10.1016/j.dadm.2017.04.003] [PMID: 28508031]
[83]
Voyle N, Baker D, Burnham SC, et al. Blood protein markers of neocortical amyloid-β burden: A candidate study using somascan technology. J Alzheimer’s Dis 2015; 46(4): 947-61.
[http://dx.doi.org/10.3233/JAD-150020] [PMID: 25881911]
[84]
Holzer P, Reichmann F, Farzi A. Neuropeptide Y, peptide YY and pancreatic polypeptide in the gut-brain axis. Neuropeptides 2012; 46(6): 261-74.
[http://dx.doi.org/10.1016/j.npep.2012.08.005] [PMID: 22979996]
[85]
Chiam JT, Dobson RJ, Kiddle SJ, Sattlecker M. Are blood-based protein biomarkers for Alzheimer’s disease also involved in other brain disorders? A systematic review. J Alzheimer’s Dis 2015; 43(1): 303-14.
[http://dx.doi.org/10.3233/JAD-140816] [PMID: 25096613]
[86]
Burnham SC, Faux NG, Wilson W, et al. A blood-based predictor for neocortical Aβ burden in Alzheimer’s disease: Results from the AIBL study. Mol Psychiatry 2014; 19(4): 519-26.
[http://dx.doi.org/10.1038/mp.2013.40] [PMID: 23628985]
[87]
Schultz N, Janelidze S, Byman E, et al. Levels of islet amyloid polypeptide in cerebrospinal fluid and plasma from patients with Alzheimer’s disease. PLoS One 2019; 14(6): e0218561.
[http://dx.doi.org/10.1371/journal.pone.0218561] [PMID: 31206565]
[88]
Solé M, Esteban-Lopez M, Taltavull B, et al. Blood-brain barrier dysfunction underlying Alzheimer’s disease is induced by an SSAO/VAP-1-dependent cerebrovascular activation with enhanced Aβ deposition. Biochim Biophys Acta Mol Basis Dis 2019; 1865(9): 2189-202.
[http://dx.doi.org/10.1016/j.bbadis.2019.04.016] [PMID: 31047972]
[89]
Solé M, Miñano-Molina AJ, Unzeta M. Cross-talk between Aβ and endothelial SSAO/VAP-1 accelerates vascular damage and Aβ aggregation related to CAA-AD. Neurobiol Aging 2015; 36(2): 762-75.
[http://dx.doi.org/10.1016/j.neurobiolaging.2014.09.030] [PMID: 25457560]
[90]
Figueiro-Silva J, Gruart A, Clayton KB, et al. Neuronal pentraxin 1 negatively regulates excitatory synapse density and synaptic plasticity. J Neurosci 2015; 35(14): 5504-21.
[http://dx.doi.org/10.1523/JNEUROSCI.2548-14.2015] [PMID: 25855168]
[91]
Ma QL, Teng E, Zuo X, et al. Neuronal pentraxin 1: A synaptic-derived plasma biomarker in Alzheimer’s disease. Neurobiol Dis 2018; 114: 120-8.
[http://dx.doi.org/10.1016/j.nbd.2018.02.014] [PMID: 29501530]
[92]
Vergallo A, Bun RS, Toschi N, et al. Association of cerebrospinal fluid α-synuclein with total and phospho-tau181 protein concentrations and brain amyloid load in cognitively normal subjective memory complainers stratified by Alzheimer’s disease biomarkers. Alzheimer’s Dement 2018; 14(12): 1623-31.
[http://dx.doi.org/10.1016/j.jalz.2018.06.3053] [PMID: 30055132]
[93]
Tofaris GK, Buckley NJ. Convergent molecular defects underpin diverse neurodegenerative diseases. J Neurol Neurosurg Psychiatry 2018; 89(9): 962-9.
[http://dx.doi.org/10.1136/jnnp-2017-316988] [PMID: 29459380]
[94]
Baldacci F, Daniele S, Piccarducci R, et al. Potential diagnostic value of red blood cells α-synuclein heteroaggregates in Alzheimer’s disease. Mol Neurobiol 2019; 56(9): 6451-9.
[http://dx.doi.org/10.1007/s12035-019-1531-4] [PMID: 30826968]
[95]
Butterfield DA, Halliwell B. Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease. Nat Rev Neurosci 2019; 20(3): 148-60.
[http://dx.doi.org/10.1038/s41583-019-0132-6] [PMID: 30737462]
[96]
Alomari E, Bruno S, Ronda L, Paredi G, Bettati S, Mozzarelli A. Protein carbonylation detection methods: A comparison. Data Brief 2018; 19: 2215-20.
[http://dx.doi.org/10.1016/j.dib.2018.06.088] [PMID: 30229098]
[97]
Greilberger J, Fuchs D, Leblhuber F, Greilberger M, Wintersteiger R, Tafeit E. Carbonyl proteins as a clinical marker in Alzheimer’s disease and its relation to tryptophan degradation and immune activation. Clin Lab 2010; 56(9-10): 441-8.
[PMID: 21086789]
[98]
Bermejo P, Martín-Aragón S, Benedí J, et al. Peripheral levels of glutathione and protein oxidation as markers in the development of Alzheimer’s disease from mild cognitive impairment. Free Radic Res 2008; 42(2): 162-70.
[http://dx.doi.org/10.1080/10715760701861373] [PMID: 18297609]
[99]
Conrad CC, Marshall PL, Talent JM, Malakowsky CA, Choi J, Gracy RW. Oxidized proteins in Alzheimer’s plasma. Biochem Biophys Res Commun 2000; 275(2): 678-81.
[http://dx.doi.org/10.1006/bbrc.2000.3356] [PMID: 10964722]
[100]
Marcello A, Wirths O, Schneider-Axmann T, Degerman-Gunnarsson M, Lannfelt L, Bayer TA. Reduced levels of IgM autoantibodies against N-truncated pyroglutamate Aβ in plasma of patients with Alzheimer’s disease. Neurobiol Aging 2011; 32(8): 1379-87.
[http://dx.doi.org/10.1016/j.neurobiolaging.2009.08.011] [PMID: 19781815]
[101]
Hughes AJ, Daniel SE, Blankson S, Lees AJ. A clinicopathologic study of 100 cases of Parkinson’s disease. Arch Neurol 1993; 50(2): 140-8.
[http://dx.doi.org/10.1001/archneur.1993.00540020018011] [PMID: 8431132]
[102]
Goetz CG, Emre M, Dubois B. Parkinson’s disease dementia: Definitions, guidelines, and research perspectives in diagnosis. Ann Neurol 2008; 64(S2)(Suppl. 2): S81-92.
[http://dx.doi.org/10.1002/ana.21455] [PMID: 19127578]
[103]
McKeith IG, Dickson DW, Lowe J, et al. Diagnosis and management of dementia with Lewy bodies: Third report of the DLB Consortium. Neurology 2005; 65(12): 1863-72.
[http://dx.doi.org/10.1212/01.wnl.0000187889.17253.b1] [PMID: 16237129]
[104]
Surmeier DJ, Guzman JN, Sanchez-Padilla J, Schumacker PT. The role of calcium and mitochondrial oxidant stress in the loss of substantia nigra pars compacta dopaminergic neurons in Parkinson’s disease. Neuroscience 2011; 198: 221-31.
[http://dx.doi.org/10.1016/j.neuroscience.2011.08.045] [PMID: 21884755]
[105]
Yu Z, Zhang S, Wang D, et al. The significance of uric acid in the diagnosis and treatment of Parkinson disease: An updated systemic review. Medicine (Baltimore) 2017; 96(45): e8502.
[http://dx.doi.org/10.1097/MD.0000000000008502] [PMID: 29137045]
[106]
Chahine LM, Stern MB, Chen-Plotkin A. Blood-based biomarkers for Parkinson’s disease. Parkinsonism Relat Disord 2014; 20(Suppl. 1): S99-S103.
[http://dx.doi.org/10.1016/S1353-8020(13)70025-7] [PMID: 24262199]
[107]
Gao X, O’Reilly ÉJ, Schwarzschild MA, Ascherio A. Prospective study of plasma urate and risk of Parkinson disease in men and women. Neurology 2016; 86(6): 520-6.
[http://dx.doi.org/10.1212/WNL.0000000000002351] [PMID: 26764029]
[108]
O’Reilly ÉJ, Gao X, Weisskopf MG, et al. Plasma urate and Parkinson’s disease in women. Am J Epidemiol 2010; 172(6): 666-70.
[http://dx.doi.org/10.1093/aje/kwq195] [PMID: 20682521]
[109]
Schapira AH. Glucocerebrosidase and Parkinson disease Recent advances Mol Cell Neurosci 2015; 66(Pt A): 37-42.
[110]
Koros C, Simitsi AM, Papagiannakis N, et al. Serum uric acid level as a putative biomarker in Parkinson’s disease patients carrying GBA1 mutations: 2-Year data from the PPMI study. Parkinsonism Relat Disord 2021; 84: 1-4.
[http://dx.doi.org/10.1016/j.parkreldis.2020.12.020] [PMID: 33508700]
[111]
Schwarzschild MA, Ascherio A, Beal MF, et al. Inosine to increase serum and cerebrospinal fluid urate in Parkinson disease: A randomized clinical trial. JAMA Neurol 2014; 71(2): 141-50.
[http://dx.doi.org/10.1001/jamaneurol.2013.5528] [PMID: 24366103]
[112]
Lin X, Cook TJ, Zabetian CP, et al. DJ-1 isoforms in whole blood as potential biomarkers of Parkinson disease. Sci Rep 2012; 2(1): 954.
[http://dx.doi.org/10.1038/srep00954] [PMID: 23233873]
[113]
Bonifati V, Rizzu P, van Baren MJ, et al. Mutations in the DJ-1 gene associated with autosomal recessive early-onset parkinsonism. Science 2003; 299(5604): 256-9.
[http://dx.doi.org/10.1126/science.1077209] [PMID: 12446870]
[114]
Maita C, Tsuji S, Yabe I, et al. Secretion of DJ-1 into the serum of patients with Parkinson’s disease. Neurosci Lett 2008; 431(1): 86-9.
[http://dx.doi.org/10.1016/j.neulet.2007.11.027] [PMID: 18162323]
[115]
Dryanovski DI, Guzman JN, Xie Z, et al. Calcium entry and α-synuclein inclusions elevate dendritic mitochondrial oxidant stress in dopaminergic neurons. J Neurosci 2013; 33(24): 10154-64.
[http://dx.doi.org/10.1523/JNEUROSCI.5311-12.2013] [PMID: 23761910]
[116]
Goedert M, Spillantini MG, Del Tredici K, Braak H. 100 years of Lewy pathology. Nat Rev Neurol 2013; 9(1): 13-24.
[http://dx.doi.org/10.1038/nrneurol.2012.242] [PMID: 23183883]
[117]
El-Agnaf OM, Salem SA, Paleologou KE, et al. Detection of oligomeric forms of α-synuclein protein in human plasma as a potential biomarker for Parkinson’s disease. FASEB J 2006; 20(3): 419-25.
[http://dx.doi.org/10.1096/fj.03-1449com] [PMID: 16507759]
[118]
Agliardi C, Meloni M, Guerini FR, et al. Oligomeric α-Syn and SNARE complex proteins in peripheral extracellular vesicles of neural origin are biomarkers for Parkinson’s disease. Neurobiol Dis 2021; 148: 105185.
[http://dx.doi.org/10.1016/j.nbd.2020.105185] [PMID: 33217562]
[119]
Tian C, Liu G, Gao L, et al. Erythrocytic α-Synuclein as a potential biomarker for Parkinson’s disease. Transl Neurodegener 2019; 8(1): 15.
[http://dx.doi.org/10.1186/s40035-019-0155-y] [PMID: 31123587]
[120]
Kikusato M, Nakamura K, Mikami Y, Mujahid A, Toyomizu M. The suppressive effect of dietary coenzyme Q10 on mitochondrial reactive oxygen species production and oxidative stress in chickens exposed to heat stress. Anim Sci J 2016; 87(10): 1244-51.
[http://dx.doi.org/10.1111/asj.12543] [PMID: 26707541]
[121]
Sohmiya M, Tanaka M, Tak NW, et al. Redox status of plasma coenzyme Q10 indicates elevated systemic oxidative stress in Parkinson’s disease. J Neurol Sci 2004; 223(2): 161-6.
[http://dx.doi.org/10.1016/j.jns.2004.05.007] [PMID: 15337618]
[122]
Isobe C, Abe T, Terayama Y. Levels of reduced and oxidized coenzyme Q-10 and 8-hydroxy-2′-deoxyguanosine in the cerebrospinal fluid of patients with living Parkinson’s disease demonstrate that mitochondrial oxidative damage and/or oxidative DNA damage contributes to the neurodegenerative process. Neurosci Lett 2010; 469(1): 159-63.
[http://dx.doi.org/10.1016/j.neulet.2009.11.065] [PMID: 19944739]
[123]
García-Moreno JM, Martin de Pablos A, García-Sánchez MI, et al. May serum levels of advanced oxidized protein products serve as a prognostic marker of disease duration in patients with idiopathic Parkinson’s disease? Antioxid Redox Signal 2013; 18(11): 1296-302.
[http://dx.doi.org/10.1089/ars.2012.5026]
[124]
Leng YP, Ma YS, Li XG, et al. l-Homocysteine-induced cathepsin V mediates the vascular endothelial inflammation in hyperhomocysteinaemia. Br J Pharmacol 2018; 175(8): 1157-72.
[http://dx.doi.org/10.1111/bph.13920] [PMID: 28631302]
[125]
Obeid R, Schadt A, Dillmann U, Kostopoulos P, Fassbender K, Herrmann W. Methylation status and neurodegenerative markers in Parkinson disease. Clin Chem 2009; 55(10): 1852-60.
[http://dx.doi.org/10.1373/clinchem.2009.125021] [PMID: 19679632]
[126]
Postuma RB, Espay AJ, Zadikoff C, et al. Vitamins and entacapone in levodopa-induced hyperhomocysteinemia: A randomized controlled study. Neurology 2006; 66(12): 1941-3.
[http://dx.doi.org/10.1212/01.wnl.0000219815.83681.f7] [PMID: 16801668]
[127]
Loeffler T, Schilcher I, Flunkert S, Hutter-Paier B. Neurofilament-light chain as biomarker of neurodegenerative and rare diseases with high translational value. Front Neurosci 2020; 14: 579.
[http://dx.doi.org/10.3389/fnins.2020.00579] [PMID: 32595447]
[128]
Hansson O, Janelidze S, Hall S, et al. Blood-based NfL: A biomarker for differential diagnosis of parkinsonian disorder. Neurology 2017; 88(10): 930-7.
[http://dx.doi.org/10.1212/WNL.0000000000003680] [PMID: 28179466]
[129]
Marques TM, van Rumund A, Oeckl P, et al. Serum NFL discriminates Parkinson disease from atypical parkinsonisms. Neurology 2019; 92(13): e1479-86.
[http://dx.doi.org/10.1212/WNL.0000000000007179] [PMID: 30814322]
[130]
Qiang JK, Wong YC, Siderowf A, et al. Plasma apolipoprotein A1 as a biomarker for Parkinson disease. Ann Neurol 2013; 74(1): 119-27.
[http://dx.doi.org/10.1002/ana.23872] [PMID: 23447138]
[131]
Li L, Liu MS, Li GQ, et al. Relationship between apolipoprotein superfamily and Parkinson’s Disease. Chin Med J (Engl) 2017; 130(21): 2616-23.
[http://dx.doi.org/10.4103/0366-6999.217092] [PMID: 29067960]
[132]
Sampaio TB, Savall AS, Gutierrez MEZ, Pinton S. Neurotrophic factors in Alzheimer’s and Parkinson’s diseases: Implications for pathogenesis and therapy. Neural Regen Res 2017; 12(4): 549-57.
[http://dx.doi.org/10.4103/1673-5374.205084] [PMID: 28553325]
[133]
Hegarty SV, O’Keeffe GW, Sullivan AM. Neurotrophic factors: From neurodevelopmental regulators to novel therapies for Parkinson’s disease. Neural Regen Res 2014; 9(19): 1708-11.
[http://dx.doi.org/10.4103/1673-5374.143410] [PMID: 25422631]
[134]
Scalzo P, Kümmer A, Bretas TL, Cardoso F, Teixeira AL. Serum levels of brain-derived neurotrophic factor correlate with motor impairment in Parkinson’s disease. J Neurol 2010; 257(4): 540-5.
[http://dx.doi.org/10.1007/s00415-009-5357-2] [PMID: 19847468]
[135]
Fan D, Pitcher T, Dalrymple-Alford J, MacAskill M, Anderson T, Guan J. Changes of plasma cGP/IGF-1 molar ratio with age is associated with cognitive status of Parkinson disease. Alzheimer’s Dement (Amst) 2020; 12(1): e12025.
[http://dx.doi.org/10.1002/dad2.12025] [PMID: 32671179]
[136]
Lim NS, Swanson CR, Cherng HR, et al. Plasma EGF and cognitive decline in Parkinson’s disease and Alzheimer’s disease. Ann Clin Transl Neurol 2016; 3(5): 346-55.
[http://dx.doi.org/10.1002/acn3.299] [PMID: 27231704]
[137]
Posavi M, Diaz-Ortiz M, Liu B, et al. Characterization of Parkinson’s disease using blood-based biomarkers: A multicohort proteomic analysis. PLoS Med 2019; 16(10): e1002931.
[http://dx.doi.org/10.1371/journal.pmed.1002931] [PMID: 31603904]
[138]
Calvani R, Picca A, Landi G, et al. A novel multi-marker discovery approach identifies new serum biomarkers for Parkinson’s disease in older people: An EXosomes in PArkiNson disease (EXPAND) ancillary study. Geroscience 2020; 42(5): 1323-34.
[http://dx.doi.org/10.1007/s11357-020-00192-2] [PMID: 32458283]
[139]
Kim R, Kim HJ, Kim A, et al. Peripheral blood inflammatory markers in early Parkinson’s disease. J Clin Neurosci 2018; 58: 30-3.
[http://dx.doi.org/10.1016/j.jocn.2018.10.079] [PMID: 30454693]
[140]
Qin XY, Zhang SP, Cao C, Loh YP, Cheng Y. Aberrations in peripheral inflammatory cytokine levels in Parkinson disease: A systematic review and meta-analysis. JAMA Neurol 2016; 73(11): 1316-24.
[http://dx.doi.org/10.1001/jamaneurol.2016.2742] [PMID: 27668667]
[141]
Calabrese V, Santoro A, Monti D, et al. Aging and Parkinson’s disease: Inflammaging, neuroinflammation and biological remodeling as key factors in pathogenesis. Free Radic Biol Med 2018; 115: 80-91.
[http://dx.doi.org/10.1016/j.freeradbiomed.2017.10.379] [PMID: 29080843]
[142]
Walker Z, Possin KL, Boeve BF, Aarsland D. Lewy body dementias. Lancet 2015; 386(10004): 1683-97.
[http://dx.doi.org/10.1016/S0140-6736(15)00462-6] [PMID: 26595642]
[143]
Gomperts SN. Lewy body dementias: Dementia with lewy bodies and Parkinson disease dementia Continuum (Minneap Minn) 2016; 22((2 Dementia)): 435-63.
[144]
Oinas M, Sulkava R, Polvikoski T, Kalimo H, Paetau A. Reappraisal of a consecutive autopsy series of patients with primary degenerative dementia: Lewy-related pathology. Acta Pathol Microbiol Scand Suppl 2007; 115(7): 820-7.
[http://dx.doi.org/10.1111/j.1600-0463.2007.apm_521.x] [PMID: 17614849]
[145]
Fujimi K, Sasaki K, Noda K, et al. Clinicopathological outline of dementia with lewy bodies applying the revised criteria: The Hisayama study. Brain Pathol 2008; 18(3): 317-25.
[http://dx.doi.org/10.1111/j.1750-3639.2008.00169.x] [PMID: 18462473]
[146]
Armstrong MJ, Sullivan JL, Amodeo K, et al. Suicide and Lewy body dementia: Report of a lewy body dementia association working group. Int J Geriatr Psychiatry 2021; 36(3): 373-82.
[147]
Vann Jones SA, O’Brien JT. The prevalence and incidence of dementia with lewy bodies: A systematic review of population and clinical studies. Psychol Med 2014; 44(4): 673-83.
[http://dx.doi.org/10.1017/S0033291713000494] [PMID: 23521899]
[148]
Hely MA, Reid WG, Adena MA, Halliday GM, Morris JG. The Sydney multicenter study of Parkinson’s disease: The inevitability of dementia at 20 years. Mov Disord 2008; 23(6): 837-44.
[http://dx.doi.org/10.1002/mds.21956] [PMID: 18307261]
[149]
Thomas AJ, Taylor JP, McKeith I, et al. Revision of assessment toolkits for improving the diagnosis of lewy body dementia: The DIAMOND lewy study. Int J Geriatr Psychiatry 2018; 33(10): 1293-304.
[http://dx.doi.org/10.1002/gps.4948] [PMID: 30091150]
[150]
Maclin JMA, Wang T, Xiao S. Biomarkers for the diagnosis of Alzheimer’s disease, dementia lewy body, frontotemporal dementia and vascular dementia. Gen Psychiatr 2019; 32(1): e100054.
[http://dx.doi.org/10.1136/gpsych-2019-100054] [PMID: 31179427]
[151]
Surendranathan A, Kane JPM, Bentley A, et al. Clinical diagnosis of Lewy body dementia. BJPsych Open 2020; 6(4): e61.
[http://dx.doi.org/10.1192/bjo.2020.44] [PMID: 32539875]
[152]
Ballard C, Aarsland D, Francis P, Corbett A. Neuropsychiatric symptoms in patients with dementias associated with cortical lewy bodies: Pathophysiology, clinical features, and pharmacological management. Drugs Aging 2013; 30(8): 603-11.
[http://dx.doi.org/10.1007/s40266-013-0092-x] [PMID: 23681401]
[153]
Bencs V, Bencze J, Módis VL, Simon V, Kálmán J, Hortobágyi T. Pathological and clinical comparison of Parkinson’s disease dementia and dementia with lewy bodies. Orv Hetil 2020; 161(18): 727-37.
[http://dx.doi.org/10.1556/650.2020.31715] [PMID: 32338488]
[154]
McKeith IG, Boeve BF, Dickson DW, et al. Diagnosis and management of dementia with lewy bodies: Fourth consensus report of the DLB Consortium. Neurology 2017; 89(1): 88-100.
[http://dx.doi.org/10.1212/WNL.0000000000004058] [PMID: 28592453]
[155]
Sokratian A, Ziaee J, Kelly K, et al. Heterogeneity in α-synuclein fibril activity correlates to disease phenotypes in lewy body dementia. Acta Neuropathol 2021; 141(4): 547-64.
[http://dx.doi.org/10.1007/s00401-021-02288-1] [PMID: 33641009]
[156]
Rizzo G, Arcuti S, Copetti M, et al. Accuracy of clinical diagnosis of dementia with Lewy bodies: A systematic review and meta-analysis. J Neurol Neurosurg Psychiatry 2018; 89(4): 358-66.
[http://dx.doi.org/10.1136/jnnp-2017-316844] [PMID: 29030419]
[157]
Caminiti SP, Sala A, Iaccarino L, et al. Brain glucose metabolism in lewy body dementia: Implications for diagnostic criteria. Alzheimer’s Res Ther 2019; 11(1): 20.
[http://dx.doi.org/10.1186/s13195-019-0473-4] [PMID: 30797240]
[158]
Ngolab J, Trinh I, Rockenstein E, et al. Brain-derived exosomes from dementia with lewy bodies propagate α-synuclein pathology. Acta Neuropathol Commun 2017; 5(1): 46.
[http://dx.doi.org/10.1186/s40478-017-0445-5] [PMID: 28599681]
[159]
van Steenoven I, van der Flier WM, Scheltens P, Teunissen CE, Lemstra AW. Amyloid-β peptides in cerebrospinal fluid of patients with dementia with lewy bodies. Alzheimer’s Res Ther 2019; 11(1): 83.
[http://dx.doi.org/10.1186/s13195-019-0537-5] [PMID: 31601267]
[160]
O’Bryant SE, Ferman TJ, Zhang F, et al. A proteomic signature for dementia with Lewy bodies. Alzheimer’s Dement (Amst) 2019; 11(1): 270-6.
[http://dx.doi.org/10.1016/j.dadm.2019.01.006] [PMID: 30923734]
[161]
Mandal PK, Pettegrew JW, Masliah E, Hamilton RL, Mandal R. Interaction between Abeta peptide and alpha synuclein: Molecular mechanisms in overlapping pathology of Alzheimer’s and Parkinson’s in dementia with lewy body disease. Neurochem Res 2006; 31(9): 1153-62.
[http://dx.doi.org/10.1007/s11064-006-9140-9] [PMID: 16947080]
[162]
Deleidi M, Maetzler W. Protein clearance mechanisms of alpha-synuclein and amyloid-beta in lewy body disorders. J Alzheimer’s Dis 2012.: 391438.
[http://dx.doi.org/10.1155/2012/391438]
[163]
Pletnikova O, West N, Lee MK, et al. Abeta deposition is associated with enhanced cortical alpha-synuclein lesions in lewy body diseases. Neurobiol Aging 2005; 26(8): 1183-92.
[http://dx.doi.org/10.1016/j.neurobiolaging.2004.10.006] [PMID: 15917102]
[164]
Bougea A, Stefanis L, Emmanouilidou E, Vekrelis K, Kapaki E. High discriminatory ability of peripheral and CFSF biomarkers in lewy body diseases. J Neural Transm (Vienna) 2020; 127(3): 311-22.
[http://dx.doi.org/10.1007/s00702-019-02137-2] [PMID: 31912280]
[165]
Chia R, Sabir MS, Bandres-Ciga S, et al. Genome sequencing analysis identifies new loci associated with lewy body dementia and provides insights into its genetic architecture. Nat Genet 2021; 53(3): 294-303.
[http://dx.doi.org/10.1038/s41588-021-00785-3] [PMID: 33589841]
[166]
Seshadri S, Fitzpatrick AL, Ikram MA, et al. Genome-wide analysis of genetic loci associated with Alzheimer disease. JAMA 2010; 303(18): 1832-40.
[http://dx.doi.org/10.1001/jama.2010.574] [PMID: 20460622]
[167]
Pankratz N, Wilk JB, Latourelle JC, et al. Genomewide association study for susceptibility genes contributing to familial Parkinson disease. Hum Genet 2009; 124(6): 593-605.
[http://dx.doi.org/10.1007/s00439-008-0582-9] [PMID: 18985386]
[168]
Sanghvi H, Singh R, Morrin H, Rajkumar AP. Systematic review of genetic association studies in people with lewy body dementia. Int J Geriatr Psychiatry 2020; 35(5): 436-48.
[http://dx.doi.org/10.1002/gps.5260] [PMID: 31898332]
[169]
Vieira RT, Caixeta L, Machado S, et al. Epidemiology of early-onset dementia: A review of the literature. Clin Pract Epidemiol Ment Health 2013; 9(1): 88-95.
[http://dx.doi.org/10.2174/1745017901309010088] [PMID: 23878613]
[170]
Bang J, Spina S, Miller BL. Frontotemporal dementia. Lancet 2015; 386(10004): 1672-82.
[http://dx.doi.org/10.1016/S0140-6736(15)00461-4] [PMID: 26595641]
[171]
Olney NT, Spina S, Miller BL. Frontotemporal Dementia. Neurol Clin 2017; 35(2): 339-74.
[http://dx.doi.org/10.1016/j.ncl.2017.01.008] [PMID: 28410663]
[172]
Swift IJ, Sogorb-Esteve A, Heller C, et al. Fluid biomarkers in frontotemporal dementia: Past, present and future. J Neurol Neurosurg Psychiatry 2021; 92(2): 204-15.
[http://dx.doi.org/10.1136/jnnp-2020-323520] [PMID: 33188134]
[173]
Sellami L, Rucheton B, Ben Younes I, et al. Plasma progranulin levels for frontotemporal dementia in clinical practice: A 10-year French experience. Neurobiol Aging 2020; 91: 167.e1-9.
[http://dx.doi.org/10.1016/j.neurobiolaging.2020.02.014] [PMID: 32171590]
[174]
Petkau TL, Leavitt BR. Progranulin in neurodegenerative disease. Trends Neurosci 2014; 37(7): 388-98.
[http://dx.doi.org/10.1016/j.tins.2014.04.003] [PMID: 24800652]
[175]
De Muynck L, Van Damme P. Cellular effects of progranulin in health and disease. J Mol Neurosci 2011; 45(3): 549-60.
[http://dx.doi.org/10.1007/s12031-011-9553-z] [PMID: 21611805]
[176]
Ntymenou S, Tsantzali I, Kalamatianos T, et al. Blood biomarkers in frontotemporal dementia: Review and meta-analysis. Brain Sci 2021; 11(2): 244.
[http://dx.doi.org/10.3390/brainsci11020244] [PMID: 33672008]
[177]
Suárez-Calvet M, Dols-Icardo O, Lladó A, et al. Plasma phosphorylated TDP-43 levels are elevated in patients with frontotemporal dementia carrying a C9orf72 repeat expansion or a GRN mutation. J Neurol Neurosurg Psychiatry 2014; 85(6): 684-91.
[http://dx.doi.org/10.1136/jnnp-2013-305972] [PMID: 24309270]
[178]
Zetterberg H, van Swieten JC, Boxer AL, Rohrer JD. Review: Fluid biomarkers for frontotemporal dementias. Neuropathol Appl Neurobiol 2019; 45(1): 81-7.
[http://dx.doi.org/10.1111/nan.12530] [PMID: 30422329]
[179]
Foulds P, McAuley E, Gibbons L, et al. TDP-43 protein in plasma may index TDP-43 brain pathology in Alzheimer’s disease and frontotemporal lobar degeneration. Acta Neuropathol 2008; 116(2): 141-6.
[http://dx.doi.org/10.1007/s00401-008-0389-8] [PMID: 18506455]
[180]
Foulds PG, Davidson Y, Mishra M, et al. Plasma phosphorylated-TDP-43 protein levels correlate with brain pathology in frontotemporal lobar degeneration. Acta Neuropathol 2009; 118(5): 647-58.
[http://dx.doi.org/10.1007/s00401-009-0594-0] [PMID: 19823856]
[181]
Yuan A, Sershen H, Veeranna ,et al. Neurofilament subunits are integral components of synapses and modulate neurotransmission and behavior in vivo. Mol Psychiatry 2015; 20(8): 986-94.
[http://dx.doi.org/10.1038/mp.2015.45] [PMID: 25869803]
[182]
Verde F, Otto M, Silani V. Neurofilament light chain as biomarker for amyotrophic lateral sclerosis and frontotemporal dementia. Front Neurosci 2021; 15: 679199.
[http://dx.doi.org/10.3389/fnins.2021.679199] [PMID: 34234641]
[183]
Rohrer JD, Woollacott IO, Dick KM, et al. Serum neurofilament light chain protein is a measure of disease intensity in frontotemporal dementia. Neurology 2016; 87(13): 1329-36.
[http://dx.doi.org/10.1212/WNL.0000000000003154] [PMID: 27581216]
[184]
van der Ende EL, Meeter LH, Poos JM, et al. Serum neurofilament light chain in genetic frontotemporal dementia: A longitudinal, multicentre cohort study. Lancet Neurol 2019; 18(12): 1103-11.
[http://dx.doi.org/10.1016/S1474-4422(19)30354-0] [PMID: 31701893]
[185]
Benussi A, Karikari TK, Ashton N, et al. Diagnostic and prognostic value of serum NfL and p-Tau181 in frontotemporal lobar degeneration. J Neurol Neurosurg Psychiatry 2020; 91(9): 960-7.
[http://dx.doi.org/10.1136/jnnp-2020-323487] [PMID: 32611664]
[186]
Ducharme S, Dols A, Laforce R, et al. Recommendations to distinguish behavioural variant frontotemporal dementia from psychiatric disorders. Brain 2020; 143(6): 1632-50.
[http://dx.doi.org/10.1093/brain/awaa018] [PMID: 32129844]
[187]
Al Shweiki MR, Steinacker P, Oeckl P, et al. Neurofilament light chain as a blood biomarker to differentiate psychiatric disorders from behavioural variant frontotemporal dementia. J Psychiatr Res 2019; 113: 137-40.
[http://dx.doi.org/10.1016/j.jpsychires.2019.03.019] [PMID: 30953863]
[188]
Katisko K, Cajanus A, Jääskeläinen O, et al. Serum neurofilament light chain is a discriminative biomarker between frontotemporal lobar degeneration and primary psychiatric disorders. J Neurol 2020; 267(1): 162-7.
[http://dx.doi.org/10.1007/s00415-019-09567-8] [PMID: 31595378]
[189]
Spotorno N, Lindberg O, Nilsson C, et al. Plasma neurofilament light protein correlates with diffusion tensor imaging metrics in frontotemporal dementia. PLoS One 2020; 15(10): e0236384.
[http://dx.doi.org/10.1371/journal.pone.0236384] [PMID: 33108404]
[190]
Meeter LH, Kaat LD, Rohrer JD, van Swieten JC. Imaging and fluid biomarkers in frontotemporal dementia. Nat Rev Neurol 2017; 13(7): 406-19.
[http://dx.doi.org/10.1038/nrneurol.2017.75] [PMID: 28621768]
[191]
Forgrave LM, Ma M, Best JR, DeMarco ML. The diagnostic performance of neurofilament light chain in CSF and blood for Alzheimer’s disease, frontotemporal dementia, and amyotrophic lateral sclerosis: A systematic review and meta-analysis. Alzheimer’s Dement (Amst) 2019; 11(1): 730-43.
[http://dx.doi.org/10.1016/j.dadm.2019.08.009] [PMID: 31909174]
[192]
Imamura K, Hishikawa N, Ono K, et al. Cytokine production of activated microglia and decrease in neurotrophic factors of neurons in the hippocampus of lewy body disease brains. Acta Neuropathol 2005; 109(2): 141-50.
[http://dx.doi.org/10.1007/s00401-004-0919-y] [PMID: 15619128]
[193]
Pasqualetti G, Brooks DJ, Edison P. The role of neuroinflammation in dementias. Curr Neurol Neurosci Rep 2015; 15(4): 17.
[http://dx.doi.org/10.1007/s11910-015-0531-7] [PMID: 25716012]
[194]
Sochocka M, Diniz BS, Leszek J. Inflammatory response in the CNS: Friend or foe? Mol Neurobiol 2017; 54(10): 8071-89.
[http://dx.doi.org/10.1007/s12035-016-0297-1] [PMID: 27889895]
[195]
Duran-Aniotz C, Orellana P, León Rodriguez T, et al. Systematic review: Genetic, neuroimaging and fluids biomarkers for frontotemporal dementia across Latin America Countries. Front Neurol 2021; 12: 663407.
[http://dx.doi.org/10.3389/fneur.2021.663407] [PMID: 34248820]
[196]
Bossù P, Salani F, Alberici A, et al. Loss of function mutations in the progranulin gene are related to pro-inflammatory cytokine dysregulation in frontotemporal lobar degeneration patients. J Neuroinflammation 2011; 8(1): 65.
[http://dx.doi.org/10.1186/1742-2094-8-65] [PMID: 21645364]
[197]
Scheller J, Chalaris A, Schmidt-Arras D, et al. The pro-and anti-inflammatory properties of the cytokine interleukin-6. Biochimica et Biophysica Acta (BBA)-. Molecular Cell Research 2011; 1813(5): 878-88.
[PMID: 21296109]
[198]
Rainero I, Rubino E, Cappa G, et al. Pro-inflammatory cytokine genes influence the clinical features of frontotemporal lobar degeneration. Dement Geriatr Cogn Disord 2009; 27(6): 543-7.
[http://dx.doi.org/10.1159/000225962] [PMID: 19546559]
[199]
Cagnin A, Rossor M, Sampson EL, Mackinnon T, Banati RB. In vivo detection of microglial activation in frontotemporal dementia. Ann Neurol 2004; 56(6): 894-7.
[http://dx.doi.org/10.1002/ana.20332] [PMID: 15562429]
[200]
Heller C, Foiani MS, Moore K, et al. Plasma glial fibrillary acidic protein is raised in progranulin-associated frontotemporal dementia. J Neurol Neurosurg Psychiatry 2020; 91(3): 263-70.
[http://dx.doi.org/10.1136/jnnp-2019-321954] [PMID: 31937580]
[201]
Katisko K, Cajanus A, Huber N, et al. GFAP as a biomarker in frontotemporal dementia and primary psychiatric disorders: Diagnostic and prognostic performance. J Neurol Neurosurg Psychiatry 2021; 92(12): 1305-12.
[http://dx.doi.org/10.1136/jnnp-2021-326487] [PMID: 34187866]
[202]
Phan K, He Y, Pickford R, et al. Uncovering pathophysiological changes in frontotemporal dementia using serum lipids. Sci Rep 2020; 10(1): 3640.
[http://dx.doi.org/10.1038/s41598-020-60457-w] [PMID: 32107421]
[203]
Katzeff JS, Bright F, Lo K, et al. Altered serum protein levels in frontotemporal dementia and amyotrophic lateral sclerosis indicate calcium and immunity dysregulation. Sci Rep 2020; 10(1): 13741.
[http://dx.doi.org/10.1038/s41598-020-70687-7] [PMID: 32792518]
[204]
Sinha K, Sun C, Kamari R, Bettermann K. Current status and future prospects of pathophysiology-based neuroprotective drugs for the treatment of vascular dementia. Drug Discov Today 2020; 25(4): 793-9.
[http://dx.doi.org/10.1016/j.drudis.2020.01.003] [PMID: 31981482]
[205]
Vijayan M, Kumar S, Bhatti JS, Reddy PH. Molecular links and biomarkers of stroke, vascular dementia, and Alzheimer’s disease. Prog Mol Biol Transl Sci 2017; 146: 95-126.
[http://dx.doi.org/10.1016/bs.pmbts.2016.12.014] [PMID: 28253992]
[206]
Takeda S, Rakugi H, Morishita R. Roles of vascular risk factors in the pathogenesis of dementia. Hypertens Res 2020; 43(3): 162-7.
[http://dx.doi.org/10.1038/s41440-019-0357-9] [PMID: 31723253]
[207]
Kalaria RN. Neuropathological diagnosis of vascular cognitive impairment and vascular dementia with implications for Alzheimer’s disease. Acta Neuropathol 2016; 131(5): 659-85.
[http://dx.doi.org/10.1007/s00401-016-1571-z] [PMID: 27062261]
[208]
Larsson SC, Markus HS. Does treating vascular risk factors prevent dementia and Alzheimer’s disease? A systematic review and meta-analysis. J Alzheimer’s Dis 2018; 64(2): 657-68.
[http://dx.doi.org/10.3233/JAD-180288] [PMID: 29914039]
[209]
Klohs J. An integrated view on vascular dysfunction in Alzheimer’s disease. Neurodegener Dis 2019; 19(3-4): 109-27.
[http://dx.doi.org/10.1159/000505625] [PMID: 32062666]
[210]
Bibl M, Esselmann H, Mollenhauer B, et al. Blood-based neurochemical diagnosis of vascular dementia: A pilot study. J Neurochem 2007; 103(2): 467-74.
[http://dx.doi.org/10.1111/j.1471-4159.2007.04763.x] [PMID: 17662050]
[211]
Lauriola M, Paroni G, Ciccone F, et al. Erythrocyte associated amyloid-β as potential biomarker to diagnose dementia. Curr Alzheimer Res 2018; 15(4): 381-5.
[http://dx.doi.org/10.2174/1567205014666171110160556] [PMID: 29125073]
[212]
He S, Zhong S, Liu G, et al. Alpha-synuclein: The interplay of pathology, neuroinflammation, and environmental factors in Parkinson’s disease. Neurodegener Dis 2021; 1-10.
[PMID: 33465773]
[213]
Barbour R, Kling K, Anderson JP, et al. Red blood cells are the major source of alpha-synuclein in blood. Neurodegener Dis 2008; 5(2): 55-9.
[http://dx.doi.org/10.1159/000112832] [PMID: 18182779]
[214]
Graham C, Santiago-Mugica E, Abdel-All Z, et al. Erythrocytes as biomarkers for dementia: Analysis of protein content and alpha-synuclein. J Alzheimer’s Dis 2019; 71(2): 569-80.
[http://dx.doi.org/10.3233/JAD-190567] [PMID: 31424413]
[215]
Wang J, Zheng B, Yang S, Hu M, Wang JH. Differential circulating levels of naturally occurring antibody to α-synuclein in Parkinson’s disease dementia, Alzheimer’s disease, and vascular dementia. Front Aging Neurosci 2020; 12: 571437.
[http://dx.doi.org/10.3389/fnagi.2020.571437] [PMID: 33088272]
[216]
Liu L, Wei H, Chen F, Wang J, Dong JF, Zhang J. Endothelial progenitor cells correlate with clinical outcome of traumatic brain injury. Crit Care Med 2011; 39(7): 1760-5.
[http://dx.doi.org/10.1097/CCM.0b013e3182186cee] [PMID: 21460712]
[217]
Balbarini A, Barsotti MC, Di Stefano R, Leone A, Santoni T. Circulating endothelial progenitor cells characterization, function and relationship with cardiovascular risk factors. Curr Pharm Des 2007; 13(16): 1699-713.
[http://dx.doi.org/10.2174/138161207780831329] [PMID: 17584100]
[218]
Kong XD, Zhang Y, Liu L, Sun N, Zhang MY, Zhang JN. Endothelial progenitor cells with Alzheimer’s disease. Chin Med J (Engl) 2011; 124(6): 901-6.
[PMID: 21518600]
[219]
Kloppenborg RP, van den Berg E, Kappelle LJ, Biessels GJ. Diabetes and other vascular risk factors for dementia: Which factor matters most? A systematic review. Eur J Pharmacol 2008; 585(1): 97-108.
[http://dx.doi.org/10.1016/j.ejphar.2008.02.049] [PMID: 18395201]
[220]
Hassing LB, Johansson B, Nilsson SE, et al. Diabetes mellitus is a risk factor for vascular dementia, but not for Alzheimer’s disease: A population-based study of the oldest old. Int Psychogeriatr 2002; 14(3): 239-48.
[http://dx.doi.org/10.1017/S104161020200844X] [PMID: 12475085]
[221]
Ott A, Stolk RP, Hofman A, van Harskamp F, Grobbee DE, Breteler MM. Association of diabetes mellitus and dementia: The Rotterdam Study. Diabetologia 1996; 39(11): 1392-7.
[http://dx.doi.org/10.1007/s001250050588] [PMID: 8933010]
[222]
Zhao L, Teter B, Morihara T, et al. Insulin-degrading enzyme as a downstream target of insulin receptor signaling cascade: Implications for Alzheimer’s disease intervention. J Neurosci 2004; 24(49): 11120-6.
[http://dx.doi.org/10.1523/JNEUROSCI.2860-04.2004] [PMID: 15590928]
[223]
Farris W, Mansourian S, Chang Y, et al. Insulin-degrading enzyme regulates the levels of insulin, amyloid beta-protein, and the beta-amyloid precursor protein intracellular domain in vivo. Proc Natl Acad Sci USA 2003; 100(7): 4162-7.
[http://dx.doi.org/10.1073/pnas.0230450100] [PMID: 12634421]
[224]
Ralat LA, Ren M, Schilling AB, Tang WJ. Protective role of Cys-178 against the inactivation and oligomerization of human insulin-degrading enzyme by oxidation and nitrosylation. J Biol Chem 2009; 284(49): 34005-18.
[http://dx.doi.org/10.1074/jbc.M109.030627] [PMID: 19808678]
[225]
Liu Z, Zhu H, Fang GG, et al. Characterization of insulin degrading enzyme and other amyloid-β degrading proteases in human serum: A role in Alzheimer’s disease? J Alzheimer’s Dis 2012; 29(2): 329-40.
[http://dx.doi.org/10.3233/JAD-2011-111472] [PMID: 22232014]
[226]
Haskó G, Linden J, Cronstein B, Pacher P. Adenosine receptors: Therapeutic aspects for inflammatory and immune diseases. Nat Rev Drug Discov 2008; 7(9): 759-70.
[http://dx.doi.org/10.1038/nrd2638] [PMID: 18758473]
[227]
Canas PM, Porciúncula LO, Cunha GM, et al. Adenosine A2A receptor blockade prevents synaptotoxicity and memory dysfunction caused by beta-amyloid peptides via p38 mitogen-activated protein kinase pathway. J Neurosci 2009; 29(47): 14741-51.
[http://dx.doi.org/10.1523/JNEUROSCI.3728-09.2009] [PMID: 19940169]
[228]
Jones PA, Smith RA, Stone TW. Protection against kainate-induced excitotoxicity by adenosine A2A receptor agonists and antagonists. Neuroscience 1998; 85(1): 229-37.
[http://dx.doi.org/10.1016/S0306-4522(97)00613-1] [PMID: 9607714]
[229]
Talukder MA, Morrison RR, Ledent C, Mustafa SJ. Endogenous adenosine increases coronary flow by activation of both A2A and A2B receptors in mice. J Cardiovasc Pharmacol 2003; 41(4): 562-70.
[http://dx.doi.org/10.1097/00005344-200304000-00008] [PMID: 12658057]
[230]
Delikouras A, Fairbanks LD, Simmonds AH, Lechler RI, Dorling A. Endothelial cell cytoprotection induced in vitro by allo- or xenoreactive antibodies is mediated by signaling through adenosine A2 receptors. Eur J Immunol 2003; 33(11): 3127-35.
[http://dx.doi.org/10.1002/eji.200323566] [PMID: 14579281]
[231]
Zhu Y, Liu L, Peng X, Ding X, Yang G, Li T. Role of adenosine A2A receptor in organ-specific vascular reactivity following hemorrhagic shock in rats. J Surg Res 2013; 184(2): 951-8.
[http://dx.doi.org/10.1016/j.jss.2013.03.039] [PMID: 23587453]
[232]
Sitkovsky MV, Lukashev D, Apasov S, et al. Physiological control of immune response and inflammatory tissue damage by hypoxia-inducible factors and adenosine A2A receptors. Annu Rev Immunol 2004; 22(1): 657-82.
[http://dx.doi.org/10.1146/annurev.immunol.22.012703.104731] [PMID: 15032592]
[233]
Gussago C, Arosio B, Casati M, et al. Different adenosine A2A receptor expression in peripheral cells from elderly patients with vascular dementia and Alzheimer’s disease. J Alzheimer’s Dis 2014; 40(1): 45-9.
[http://dx.doi.org/10.3233/JAD-131652] [PMID: 24321892]
[234]
Sodhi CP, Phadke SA, Batlle D, Sahai A. Hypoxia and high glucose cause exaggerated mesangial cell growth and collagen synthesis: Role of osteopontin. Am J Physiol Renal Physiol 2001; 280(4): F667-74.
[http://dx.doi.org/10.1152/ajprenal.2001.280.4.F667] [PMID: 11249858]
[235]
Golledge J, McCann M, Mangan S, Lam A, Karan M. Osteoprotegerin and osteopontin are expressed at high concentrations within symptomatic carotid atherosclerosis. Stroke 2004; 35(7): 1636-41.
[http://dx.doi.org/10.1161/01.STR.0000129790.00318.a3] [PMID: 15143295]
[236]
Ellison JA, Velier JJ, Spera P, et al. Osteopontin and its integrin receptor alpha(v)beta3 are upregulated during formation of the glial scar after focal stroke. Stroke 1998; 29(8): 1698-706.
[http://dx.doi.org/10.1161/01.STR.29.8.1698] [PMID: 9707214]
[237]
Hosaka K, Rojas K, Fazal HZ, et al. Monocyte chemotactic protein-1-interleukin-6-osteopontin pathway of intra-aneurysmal tissue healing. Stroke 2017; 48(4): 1052-60.
[http://dx.doi.org/10.1161/STROKEAHA.116.015590] [PMID: 28292871]
[238]
Uchibori T, Matsuda K, Shimodaira T, Sugano M, Uehara T, Honda T. IL-6 trans-signaling is another pathway to upregulate Osteopontin. Cytokine 2017; 90: 88-95.
[http://dx.doi.org/10.1016/j.cyto.2016.11.006] [PMID: 27863335]
[239]
Scatena M, Liaw L, Giachelli CM. Osteopontin: A multifunctional molecule regulating chronic inflammation and vascular disease. Arterioscler Thromb Vasc Biol 2007; 27(11): 2302-9.
[http://dx.doi.org/10.1161/ATVBAHA.107.144824] [PMID: 17717292]
[240]
Chai YL, Chong JR, Raquib AR, et al. Plasma osteopontin as a biomarker of Alzheimer’s disease and vascular cognitive impairment. Sci Rep 2021; 11(1): 4010.
[http://dx.doi.org/10.1038/s41598-021-83601-6] [PMID: 33597603]

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