[1]
Burns A, Iliffe S. Alzheimer’s disease. BMJ 338: b158. (2009)
[2]
Seltzer B, Sherwin I. A comparison of clinical features in early- and late-onset primary degenerative dementia. One entity or two? Arch Neurol 40(3): 143-6. (1983)
[3]
Schmidt C, Redyk K, Meissner B, Krack L, von Ahsen N, Roeber S, et al. Clinical features of rapidly progressive Alzheimer’s disease. Dement Geriatr Cogn Disord 29(4): 371-8. (2010)
[4]
Schmidt C, Wolff M, Weitz M, Bartlau T, Korth C, Zerr I. Rapidly progressive Alzheimer disease. Arch Neurol 68: 1124-30. (2011)
[5]
Persson K, Eldholm RS, Barca ML, Cavallin L, Ferreira D, Knapskog AB, et al. MRI-assessed atrophy subtypes in Alzheimer’s disease and the cognitive reserve hypothesis. PLoS One 12e0186595 (2017)
[6]
Park JY, Na HK, Kim S, Kim H, Kim HJ, Seo SW, et al. Robust identification of Alzheimer's disease subtypes based on cortical atrophy patterns. 7: 43270 (2017)
[7]
Squitti R, Simonelli I, Cassetta E, Lupoi D, Rongioletti M, Ventriglia M, et al. Patients with increased non-ceruloplasmin copper appear a distinct sub-group of Alzheimer’s disease: a neuroimaging study. Curr Alzheimer Res 14(12): 1318-26. (2017)
[8]
K. Iqbal, M. Flory, S. Khatoon, H. Soininen, T. Pirttila, M. Lehtovirta, et al. Subgroups of Alzheimer’s disease based on cerebrospinal fluid molecular markers. Ann Neurol 58: 748-57. (2005)
[9]
M. Li, H. Li, G. Hong, Z. Tang, G. Liu, X. Lin, et al. Identifying primary site of lung-limited Cancer of unknown primary based on relative gene expression orderings. BMC Cancer 19: 67. (2019)
[10]
Hong G, Li H, Li M, Zheng W, Li J, Chi M, et al. A simple way to detect disease-associated cellular molecular alterations from mixed-cell blood samples. Brief Bioinform 19: 613-21. (2018)
[11]
Berchtold NC, Cribbs DH, Coleman PD, Rogers J, Head E, Kim R, et al. Gene expression changes in the course of normal brain aging are sexually dimorphic. Proc Natl Acad Sci USA 105: 15605-10. (2008)
[12]
Berchtold NC, Coleman PD, Cribbs DH, Rogers J, Gillen DL, Cotman CW. Synaptic genes are extensively downregulated across multiple brain regions in normal human aging and Alzheimer’s disease. Neurobiol Aging 34: 1653-61. (2013)
[13]
Benjamini Y, Hochberg Y. Controlling the false discovery rate: a practical and powerful approach to multiple testing. J Royal Stats Soc: Series B (Methodological) 57: 289-300. (1995)
[14]
Shoffner JM. Oxidative phosphorylation defects and Alzheimer’s disease. Neurogenetics 1: 13-9. (1997)
[15]
Keller JN, Hanni KB, Markesbery WR. Impaired proteasome function in Alzheimer’s disease. J Neurochem 75: 436-9. (2000)
[16]
Bonet-Costa V, Pomatto LC, Davies KJ. The proteasome and oxidative stress in Alzheimer’s disease. Antioxid Redox Signal 25: 886-901. (2016)
[17]
Ovsepian SV, O’Leary VB, Zaborszky L, Ntziachristos V, Dolly JO. Synaptic vesicle cycle and amyloid beta: biting the hand that feeds. Alzheimers Dement 14: 502-13. (2018)
[18]
Hochstrasser T, Weiss E, Marksteiner J, Humpel C. Soluble cell adhesion molecules in monocytes of Alzheimer’s disease and mild cognitive impairment. Exp Gerontol 45(1): 70-4. (2010)
[19]
Marlow L, Cain M, Pappolla MA, Sambamurti K. Beta-secretase processing of the Alzheimer’s amyloid protein precursor (APP). J Mol Neurosci 20(3): 233-9. (2003)
[20]
Berridge MJ. Dysregulation of neural calcium signaling in Alzheimer disease, bipolar disorder and schizophrenia. Prion 7: 2-13. (2013)
[21]
Afanador L, Roltsch EA, Holcomb L, Campbell KS, Keeling DA, Zhang Y, et al. The Ca2+ sensor S100A1 modulates neuroinflammation, histopathology and Akt activity in the PSAPP Alzheimer’s disease mouse model. Cell Calcium 56: 68-80. (2014)
[22]
Afanador L, Keeling D, Campbell K, Campbell K, Roltsch E, Zimmer D. Aberrant calcium signaling modulates inflammatory and PI3/Akt pathways in Alzheimer’s disease. Alzheimers Dement 9: 352-52. (2013)
[23]
Akiyama H. Inflammatory response in Alzheimer’s disease. Tohoku J Exp Med 174: 295-303. (1994)
[24]
Biron KE, Dickstein DL, Gopaul R, Jefferies WA. Amyloid triggers extensive cerebral angiogenesis causing blood brain barrier permeability and hypervascularity in Alzheimer’s disease. PLoS One 6e23789 (2011)
[25]
Roberts TK, Eugenin EA, Lopez L, Romero IA, Wekslee BB, Couraud PO, et al. CCL2 disrupts the adherens junction: implications for neuroinflammation. Lab Invest 92: 1213-33. (2012)
[26]
Ostan R, Lanzarini C, Pini E, Scurti M, Vianello D, Bertarelli C, et al. Inflammaging and cancer: a challenge for the Mediterranean diet. Nutrients 7: 2589-621. (2015)
[27]
Piemontese L. An innovative approach for the treatment of Alzheimer’s disease: the role of peroxisome proliferator-activated receptors and their ligands in development of alternative therapeutic interventions. Neural Regen Res 14: 43-5. (2019)
[28]
Song J, Lee JE. Adiponectin as a new paradigm for approaching Alzheimer’s disease. Anat Cell Biol 46: 229-34. (2013)
[29]
Jin JJ, Kim HD, Maxwell JA, Li L, Fukuchi K. Toll-like receptor 4-dependent upregulation of cytokines in a transgenic mouse model of Alzheimer’s disease. J Neuroinflammation 5: 23. (2008)
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