Abstract
Background: Alzheimer's disease (AD) is the most common and well-studied neurodegenerative disease (ND). Biological pathways, pathophysiology and genetics of AD show commonalities with other NDs viz. Parkinson's disease (PD), Amyotrophic lateral sclerosis (ALS), Huntington's disease (HD), Prion disease and Dentatorubral-pallidoluysian atrophy (DRPLA). Many of the NDs, sharing the common features and molecular mechanisms suggest that pathology may be directly comparable and be implicated in disease prevention and development of highly effective therapies.
Method: In this review, a brief description of pathophysiology, clinical symptoms and available treatment of various NDs have been explored with special emphasis on AD. Commonalities in these fatal NDs provide support for therapeutic advancements and enhance the understanding of disease manifestation.
Conclusion: The studies concentrating on the commonalities in biological pathways, cellular mechanisms and genetics may provide the scope to researchers to identify few novel common target(s) for disease prevention and development of effective common drugs for multi-neurodegenerative diseases.
Keywords: Neurodegenerative diseases, Alzheimer disease, Parkinson's disease, Huntington's disease, Amyotrophic lateral sclerosis, biological pathways.
[1]
Silberberg D. The high impact of neurologic disorders in developing countries: the struggle for global recognition. Neurology 77(3): 307-8. (2011).
[2]
Pedro AV. Coping with Brain Disorders using Neurotechnology. Malays J Med Sci 19(1): 1-3. (2012).
[3]
Teplow DB. Molecular biology of neurodegenerative diseases. Preface. Prog Mol Biol Transl Sci 107: xiii-v. (2012).
[4]
Gao HM, Hong JS. Why neurodegenerative diseases are progressive: uncontrolled inflammation drives disease progression. Trends Immunol 29(8): 357-65. (2008).
[5]
Kruttgen A, Saxena S, Evangelopoulos ME, Weis J. Neurotrophins and neurodegenerative diseases: receptors stuck in traffic? J Neuropathol Exp Neurol 62(4): 340-50. (2003).
[6]
Ahmad K, Balaramnavar VM, Baig MH, Srivastava AK, Khan S, Kamal MA. Identification of potent caspase-3 inhibitors for treatment of multi- neurodegenerative diseases using pharmacophore modeling and docking approaches. CNS Neurol Disord Drug Targets 13(8): 1346-53. (2014).
[7]
Jellinger KA. Formation and development of Lewy pathology: a critical update. J Neurol 256(3): 270-9. (2009).
[8]
Brookmeyer R, Johnson E, Ziegler-Graham K, Arrighi HM. Forecasting the global burden of Alzheimer’s disease. Alzheimers Dement 3(3): 186-91. (2007).
[9]
Przedborski S, Vila M, Jackson-Lewis V. Neurodegeneration: what is it and where are we? J Clin Invest 111(1): 3-10. (2003).
[10]
Martin JB. Molecular basis of the neurodegenerative disorders. N Engl J Med 340(25): 1970-80. (1999).
[11]
Hebert LE, Beckett LA, Scherr PA, Evans DA. Annual incidence of Alzheimer disease in the United States projected to the years 2000 through 2050. Alzheimer Dis Assoc Disord 15(4): 169-73. (2001).
[12]
Hebert LE, Scherr PA, Bienias JL, Bennett DA, Evans DA. Alzheimer disease in the US population: prevalence estimates using the 2000 census. Arch Neurol 60(8): 1119-22. (2003).
[13]
Russell A, Drozdova A, Wang W, Thomas M. The impact of dementia development concurrent with Parkinson’s disease: a new perspective. CNS Neurol Disord Drug Targets 13(7): 1160-8. (2014).
[14]
Cavalli A, Bolognesi ML, Minarini A, Rosini M, Tumiatti V, Recanatini M, et al. Multi-target-directed ligands to combat neurodegenerative diseases. J Med Chem 51(3): 347-72. (2008).
[15]
Rizzi L, Rosset I, Roriz-Cruz M. Global epidemiology of dementia: Alzheimer’s and vascular types. Biomed Res Int 2014: 908915 (2014).
[16]
Terry RD, Peck A, DeTeresa R, Schechter R, Horoupian DS. Some morphometric aspects of the brain in senile dementia of the Alzheimer type. Ann Neurol 10(2): 184-92. (1981).
[18]
Masliah E, Mallory M, Alford M, DeTeresa R, Iwai A, Saitoh T. Molecular Mechanisms of Synaptic Disconnection in Alzheimer’s Disease. In: Connections, Cognition and Alzheimer’s Disease. (Eds: Hayman BT, Duyckaerts C, Christen Y). Berlin, Heidelberg: Springer Berlin Heidelberg; pp. 121-40 (1997).
[20]
LaFerla FM, Oddo S. Alzheimer’s disease: Abeta, tau and synaptic dysfunction. Trends Mol Med 11(4): 170-6. (2005).
[21]
Kang J, Lemaire HG, Unterbeck A, Salbaum JM, Masters CL, Grzeschik KH, et al. The precursor of Alzheimer’s disease amyloid A4 protein resembles a cell-surface receptor. Nature 325(6106): 733-6. (1987).
[22]
Chartier-Harlin MC, Crawford F, Houlden H, Warren A, Hughes D, Fidani L, et al. Early-onset Alzheimer’s disease caused by mutations at codon 717 of the beta-amyloid precursor protein gene. Nature 353(6347): 844-6. (1991).
[23]
Goate A, Chartier-Harlin MC, Mullan M, Brown J, Crawford F, Fidani L, et al. Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer’s disease. Nature 349(6311): 704-6. (1991).
[24]
Citron M, Oltersdorf T, Haass C, McConlogue L, Hung AY, Seubert P, et al. Mutation of the beta-amyloid precursor protein in familial Alzheimer’s disease increases beta-protein production. Nature 360(6405): 672-4. (1992).
[25]
Games D, Adams D, Alessandrini R, Barbour R, Berthelette P, Blackwell C, et al. Alzheimer-type neuropathology in transgenic mice overexpressing V717F beta-amyloid precursor protein. Nature 373(6514): 523-7. (1995).
[26]
Cole SL, Vassar R. The Alzheimer’s disease beta-secretase enzyme, BACE1. Mol Neurodegener 2: 22. (2007).
[27]
Suzuki N, Cheung TT, Cai XD, Odaka A, Otvos L Jr, Eckman C, et al. An increased percentage of long amyloid beta protein secreted by familial amyloid beta protein precursor (beta APP717) mutants. Science 264(5163): 1336-40. (1994).
[28]
Adlard PA, Cummings BJ. Alzheimer’s disease--a sum greater than its parts? Neurobiol Aging 25(6): 725-733; discussion 43-6. (2004).
[29]
Holscher C. Possible causes of Alzheimer’s disease: amyloid fragments, free radicals, and calcium homeostasis. Neurobiol Dis 5(3): 129-41. (1998).
[30]
Bolognesi ML, Banzi R, Bartolini M, Cavalli A, Tarozzi A, Andrisano V, et al. Novel class of quinone-bearing polyamines as multi-target-directed ligands to combat Alzheimer’s disease. J Med Chem 50(20): 4882-97. (2007).
[31]
Gotz J, Schild A, Hoerndli F, Pennanen L. Amyloid-induced neurofibrillary tangle formation in Alzheimer’s disease: insight from transgenic mouse and tissue-culture models. Int J Dev Neurosci 22(7): 453-65. (2004).
[32]
Waite LM. Treatment for Alzheimer’s disease: has anything changed? Aust Prescr 38(2): 60-3. (2015).
[33]
Lev N, Melamed E, Offen D. Apoptosis and Parkinson’s disease. Prog Neuropsychopharmacol Biol Psychiatry 27(2): 245-50. (2003).
[34]
Corti O, Hampe C, Darios F, Ibanez P, Ruberg M, Brice A. Parkinson’s disease: from causes to mechanisms. C R Biol 328(2): 131-42. (2005).
[35]
Booth TC, Nathan M, Waldman AD, Quigley AM, Schapira AH, Buscombe J. The role of functional dopamine-transporter SPECT imaging in parkinsonian syndromes, part 1. AJNR Am J Neuroradiol 36(2): 229-35. (2015).
[36]
Shastry BS. Parkinson disease: etiology, pathogenesis and future of gene therapy. Neurosci Res 41(1): 5-12. (2001).
[38]
Payami H, Factor SA. Promise of pharmacogenomics for drug discovery, treatment and prevention of Parkinson’s disease. A perspective. Neurotherapeutics 11(1): 111-6. (2014).
[39]
Goodman AO, Murgatroyd PR, Medina-Gomez G, Wood NI, Finer N, Vidal-Puig AJ, et al. The metabolic profile of early Huntington’s disease--a combined human and transgenic mouse study. Exp Neurol 210(2): 691-8. (2008).
[40]
Kim HS, Lyoo CH, Lee PH, Kim SJ, Park MY, Ma HI, et al. Current Status of Huntington’s Disease in Korea: A Nationwide Survey and National Registry Analysis. J Mov Disord 8(1): 14-20. (2015).
[41]
Block RC, Dorsey ER, Beck CA, Brenna JT, Shoulson I. Altered cholesterol and fatty acid metabolism in Huntington disease. J Clin Lipidol 4(1): 17-23. (2010).
[42]
Fink KD, Deng P, Torrest A, Stewart H, Pollock K, Gruenloh W, et al. Developing stem cell therapies for juvenile and adult-onset Huntington’s disease. Regen Med 10(5): 623-46. (2015).
[44]
Hayashi Y, Kakita A, Yamada M, Egawa S, Oyanagi S, Naito H, et al. Hereditary dentatorubral-pallidoluysian atrophy: ubiquitinated filamentous inclusions in the cerebellar dentate nucleus neurons. Acta Neuropathol 95(5): 479-82. (1998).
[45]
Igarashi S, Koide R, Shimohata T, Yamada M, Hayashi Y, Takano H, et al. Suppression of aggregate formation and apoptosis by transglutaminase inhibitors in cells expressing truncated DRPLA protein with an expanded polyglutamine stretch. Nat Genet 18(2): 111-7. (1998).
[46]
Simpson CL, Al-Chalabi A. Amyotrophic lateral sclerosis as a complex genetic disease. Biochim Biophys Acta 1762(11-12): 973-85. (2006).
[48]
Phukan J, Pender NP, Hardiman O. Cognitive impairment in amyotrophic lateral sclerosis. Lancet Neurol 6(11): 994-1003. (2007).
[49]
Mohan RD, Abmayr SM, Workman JL. The expanding role for chromatin and transcription in polyglutamine disease. Curr Opin Genet Dev 26: 96-104. (2014).
[51]
Karapetyan YE, Sferrazza GF, Zhou M, Ottenberg G, Spicer T, Chase P, et al. Unique drug screening approach for prion diseases identifies tacrolimus and astemizole as antiprion agents. Proc Natl Acad Sci USA 110(17): 7044-9. (2013).
[52]
Kayed R, Head E, Thompson JL, McIntire TM, Milton SC, Cotman CW, et al. Common structure of soluble amyloid oligomers implies common mechanism of pathogenesis. Science 300(5618): 486-9. (2003).
[53]
Bossy-Wetzel E, Schwarzenbacher R, Lipton SA. Molecular pathways to neurodegeneration. Nat Med 10: S2-9. (2004).
[54]
Ross CA, Poirier MA. Protein aggregation and neurodegenerative disease. Nat Med 10: S10-7. (2004).
[55]
Kamal MA, Mushtaq G, Greig NH. Current Update on Synopsis of miRNA Dysregulation in Neurological Disorders. CNS Neurol Disord Drug Targets 14(4): 492-501. (2015).
[57]
Dobson CM. Protein misfolding, evolution and disease. Trends Biochem Sci 24(9): 329-32. (1999).
[58]
Soto C. Protein misfolding and disease; protein refolding and therapy. FEBS Lett 498(2-3): 204-7. (2001).
[60]
Selkoe DJ. Alzheimer’s disease: genes, proteins, and therapy. Physiol Rev 81(2): 741-66. (2001).
[62]
Ince PG, Highley JR, Kirby J, Wharton SB, Takahashi H, Strong MJ, et al. Molecular pathology and genetic advances in amyotrophic lateral sclerosis: an emerging molecular pathway and the significance of glial pathology. Acta Neuropathol 122(6): 657-71. (2011).
[63]
Grunblatt E. Commonalities in the genetics of Alzheimer’s disease and Parkinson’s disease. Expert Rev Neurother 8(12): 1865-77. (2008).
[64]
Giau VV, Bagyinszky E, An SS, Kim SY. Role of apolipoprotein E in neurodegenerative diseases. Neuropsychiatr Dis Treat 11: 1723-37. (2015).
[65]
Mathisen PM. Gene discovery and validation for neurodegenerative diseases. Drug Discov Today 8(1): 39-46. (2003).
[66]
Goehler H, Lalowski M, Stelzl U, Waelter S, Stroedicke M, Worm U, et al. A protein interaction network links GIT1, an enhancer of huntingtin aggregation, to Huntington’s disease. Mol Cell 15(6): 853-65. (2004).
[67]
Giorgini F, Muchowski PJ. Connecting the dots in Huntington’s disease with protein interaction networks. Genome Biol 6(3): 210. (2005).
[69]
Rhodes DR, Chinnaiyan AM. Integrative analysis of the cancer transcriptome. Nat Genet 37: S31-7. (2005).
[70]
Gunsalus KC, Ge H, Schetter AJ, Goldberg DS, Han JD, Hao T, et al. Predictive models of molecular machines involved in Caenorhabditis elegans early embryogenesis. Nature 436(7052): 861-5. (2005).
[71]
Goh KI, Cusick ME, Valle D, Childs B, Vidal M, Barabasi AL. The human disease network. Proc Natl Acad Sci USA 104(21): 8685-90. (2007).
[72]
Jin L, Zuo XY, Su WY, Zhao XL, Yuan MQ, Han LZ, et al. Pathway-based analysis tools for complex diseases: a review. Genomics Proteomics Bioinformatics 12(5): 210-20. (2014).
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