Review on Aetiology, Diagnosis and Treatment of Alzheimer’s disease
Alzheimer’s disease (AD) is one of the most common cause of dementia in older adults and an important public health problem. The purpose of this review article is to provide a brief introduction to A D and the related concept of mild cognitive impairment (M C I) and may throw light on the prevalence, causes, treatment, diagnosis and prevention. Vast knowledge regarding disease and disorders will help people take precautions for not getting effected by it. This will help reduce the number of Alzheimer’s disease. Since the exact curative treatment has not been established for AD. AD is a complex disorder with environmental and genetic components. There are two major types of Alzheimer’s disease, early on set and the more common late onset. The genetics of early-onset Alzheimer’s disease are largely understood with variants in three different genes leading to AD disease. In contrast, with several common alleles associated with late-onset Alzheimer’s disease, including APOE, have been identified using association studies, the genetics of late-onset Alzheimer’s disease are not fully understood. Continuing efforts are still required. This includes development of medicines that would slow progression, halt, or prevent AD and other dementias from occurring. Studies are currently underway to identify biomarkers for diagnosis and new therapeutical agents to prevent or slow down disease progression.
Keywords: Alzheimer’s disease, dementia, neuro-degeneration, mild cognitive impairment.
2. Mark T, Perry G. Review Article Genetics of Alzheimer’s disease. Bio Med Research International.2013; 7(1):1-13.
3. Gross A, Jones R, Habtemariam D, Fong T, Tommet D, Quach L, Schmitt E, Yap L, Inouye SK. Delirium and Long-term Cognitive Trajectory Among Persons With Dementia. Arch Intern Med. 2012; 172(17):1324-31.
4. Sheldon F, Shaffer J, Petrella J, Choudhury K, Calhoun V, Coleman R, Doraiswamy P. alzheimer’s Disease Neuroimaging Initiative. Predicting Cognitive Decline in Subjects at Risk for Alzheimer Disease by Using Combined Cerebrospinal Fluid, MR Imaging, and PET Biomarkers. Radiology. 2013; 266(2):583-91.
5. Alzheimer A. Uber eine eigenartige Erkrankung der Hirnridne. About a Peculiar Disease of the Cerebral Cortex. Allg Z Psychiatr. 1907; 64: 146-48.
6. Alzheimer A. About a peculiar disease of the cerebral cortex. Alzheimer Dis Assoc Disord. 1987; 1(3); 8.
7. Maurer K, Volk S, Gerbaldo H. Auguste D and Alzheimer’s disease. Lancet .1997; 349(9064): 1546.
8. Alan J. Lerner, Women and Alzheimer’s disease. The Journal of Clinical Endocrinology & Metabolism. 1999; 84(6); 1830-1834.
9. Edith, Samuel. Recent Research and Updates on Alzheimer’s disease. Journal of Psychology and Behavioural Science.2014; 2(2); 103-12.
10. Korole v, Igor O. Alzheimer’s disease. A Clinical and Basic Science Review. Medical Student Research Journal; 2014; 04(9); 024-033.
11. Reshma H .Alzheimer's Disease- A Review, J. Pharm. Sci. & Res.2016; 8(11): 1292-94.
12. Gilman S. Oxford American handbook of neurology. Oxford University Press: Oxford, UK; 2010.ISBN 10: 0195369793 ISBN 13: 9780195369793.
13. Hyman B , Jack C , Kawas C , McKhann G , Knopman D, Chertkow H. The diagnosis of dementia due to Alzheimer’s disease: recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement .2011; 7(3):26-39.
14. Seeley W, Kim E , Rabinovici G D, Gorno-Tempini M L, Rascovsky K, Pagliaro TA. Distinct MRI atrophy patterns in autopsy-proven Alzheimer’s disease and front to temporal lobar degeneration.Am J Alzheimers Dis Other Dement .2007; 22:474-88.
15. Van Broeckhoven C, Van Cauwenberghe C, Sleegers K. The genetic landscape of Alzheimer disease. Clinical implications and perspectives. Genet Med. 2016; 18:421-30.
16. Filley C M. Alzheimer's disease in women. Am J Obstet Gynecol. 1997; 176:1-7.
17. Bass M P, Pericak-Vance MA, Yamaoka LH. Complete genomic screen in late-onset familial Alzheimer's disease: evidence for a new locus on chromosome 12. JAMA. 1997; 278:1237-41.
18. Hardy J. The Alzheimer family of diseases: many etiologies, one pathogenesis Proc Natl Acad Sci USA. 1997; 94:2095-97.
19. Singh V K. Neuroautoimmunity: pathogenic implications for Alzhei- mer's disease. Gerontology. 1997; 43:79-89.
20. Singer S J, Delvji N N. Genetic clues to Alzheimer's disease. Science. 1996; 271:159-60.
21. Lendon C, Goate A M, Ashall F. Exploring the etiology of Alzheimer disease using molecular genetics. JAM. 1997; 277:825-31.
22. Hasegawa M. Molecular Mechanisms in the Pathogenesis of Alzheimer’s disease and Tauopathies-Prion-Like Seeded Aggregation and Phosphorylation. Biomolecules. 2016; 6(2):24.
23. Schöll M, Hansson O, Zetterberg H ,Blennow K, Mattsson N. Amyloid biomarkers in Alzheimer’s disease. Trends Pharmacol Sci. 2015; 36:297-09.
24. Barage S H, Sonawane, K D. Amyloid cascade hypothesis: Pathogenesis and therapeutic strategies in Alzheimer’s disease. Neuropeptides. 2015; 52:1-18.
25. Khan A, Kalra J. Reducing AÎ² load and tau phosphorylation: Emerging perspective for treating Alzheimer’s disease. Eur J Pharmacol. 2015; 764:571-581.
26. Singh B, Anand P. A review on cholinesterase inhibitors for Alzheimer’s disease. Arch Pharm Res. 2013; 36: 375-99.
27. Jellinger K A. Basic mechanisms of neurodegeneration: a critical update. J Cell Mol Med. 2010; 14:457-87.
28. Saykin, Ramanan VK. Pathways to neurodegeneration: mechanistic insights from GWAS in Alzheimer´s disease, Parkinson´s disease, and related disorders. Am J Neurodegener Dis. 2013; 2:145-75.
29. Beal M F, Lin M T. Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases. Nature. 2006; 443:787-95.
30. Harrison F E Walker J M. Shared Neurophatological Characteristics of Obesity, Type 2 Diabetes and Alzheimer´s Disease: Impacts on Cognitive Decline. Nutrients. 2015; 7: 7332-57.
31. Mattson M P, Kapogiannis D. Disrupted energy metabolism and neuronal circuit dysfunction in cognitive impairment and Alzheimer’s disease. Lancet Neurol. 2011; 10: 187-98.
32. Marschoff E R, Gonzalez S E Domínguez R O, Pagano M A, Repetto M G, et al. Alzheimer disease and cognitive impairment associated with diabetes mellitus type 2 associations and hypothesis. Neurología. 2014; 29:567-72.
33. Soiza R L, Kelleher R J. Evidence of endothelial dysfunction in the development of Alzheimer’s disease: Is Alzheimer’s a vascular disorder. Am J Cardiovasc Dis. 2013; 3:197-26.
34. Karran E, De Strooper B. The Cellular Phase of Alzheimer’s disease. Cell. 2016; 164:603-15.
35. Di Marco LY, , Evans PC, Marzo A ,Venneri A, Farkas E. Neurobiology of Disease Vacular dysfunction in the pathogenesis of Alzheimer´s disease – A review of endothelium mediated mechanisms and ensuing vicious circles. Neurobiol Dis. 2015; 82:593-606.
36. Janota C, Brito M A, Lemere CA. Dissecting the Contribution of Vascular Alterations and Aging to Alzheimer’s disease. Mol Neurobiol. 2016; 53: 3793-811.
37. Busse A. Mild cognitive impairment long-term course of four clinical subtypes. Neurology.2006. 67(12):2176-85.
38. Tanzi R E, Bertram L. The genetic epidemiology of neurodegenerative disease. J Clin Invest. 2005; 115:1449-57.
39. Coppedè F, Migliore L. Genetics, environmental factors and the emerging role of epigenetics in neurodegenerative diseases. Mutat Res. 2009; 667: 82-97.
40. Andrew J Saykin, Vijay K. Pathways to neurodegeneration: mechanistic insights from GWAS in Alzheimer’s disease, Parkinson’s disease, and related disorders. Am J Neurodegener Dis 2013; 2(3):145-75.
41. Nestler EJ, Malenka RC, Hyman SE. Molecular Neuropharmacology: Neurodegeneration. China: McGraw-Hill. 2009.
42. Di Mauro S, Schon EA. Mitochondrial disorders in the nervous system`Annu Rev Neurosci. 2008; 31:91-123.
43. Glass C K, Saijo K, Gage F H, Winner B, Marchetto MC. Mechanisms underlying inflammation in neurodegeneration. Cell. 2010; 140: 918-34.
44. Richard Mayeux and Yaakov Stern .Epidemiology of Alzheimer Disease. Stern Cold Spring Harb Perspect Med 2012; 2(8):1-18.
45. Lendon C L, Goate A M, Ashall F. Exploring the aetiology of Alzheimer disease using molecular genetics. JAM. 1997; 277:825-31.
46. Gilnian S. Alzheimer's disease. Perspect Biol filed. 1997; 40:230-45.
47. Knight J A. Reactive oxygen species and the neurodegenerative disorders. Am Clin Lab Sci. 1997; 27:11-25.
48. Saunders AM, Strittmatter WJ. “Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer’s disease in late onset families,”Science.1993; 261(.5123):921– 23.
49. Hendrie HC, Hui S, Hall KS, Apolipoprotein E genotypes and Alzheimer’s disease in a community study of Bio Med Research International 9 elderly African Americans,”Annals of Neurology;1995;37(1):118–20.
50. Ottman GR, Stern Y. “Apolipoprotein E and Alzheimer’s disease: ethnic variation in genotypic risks,”Annals of Neurology.1995; 37(2):254–59.
51. Noguchi S, Yamada N, K. Murakami. “Apolipoprotein E genotype and Alzheimer’s disease,” The Lancet; 1993; 342(8873):737–38.
52. Kawano M, Ueki A, Namba Y, Kawakami M, and Ikeda K. “A high frequency of apolipoprotein E4 isoprotein in Japanese patients with late-onset non familial Alzheimer’s disease, Neuroscience Letters. 1993; 163(2):166–68.
53. Abraham, D. Harold, P. Holling worth. “Genome wide association study identifies variant sat CLU and PICALM associated with Alzheimer’s disease. Nature Genetics.2009; 41:1088–93.
54. Corder EH, Risch NJ, Saunders AM. “Protective effect of apolipo-protein E type 2 allele for late onset Alzheimer disease .Nature Genetics.1994; 7(2):180–84.
55. Mc Khann. The diagnosis of dementia due to Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimer's & dementia. 2011; 7(3): 263-69.
56. Braak H, Thal D R, Del Tredici K, Ghebremedhin E. Stages of the pathologic process in Alzheimer disease: age categories from 1 to 100 years. J Neuropathol Exp Neurol 2011; 70:96-09.
57. Guhne U, Busse A, Hensel A, Angermeyer MC, Riedel-Heller SG. Mild cognitive impairment: long-term course of four clinical subtypes. Neurology .2006; 67:217685.
58. Weigand S D, Shaw L M ,Vemuri P, Wiste H J, Trojanowski J Q, Weiner M W. MRI and CSF biomarkers in normal, MCI, and AD subjects: diagnostic discrimination and cognitive correlations. Neurology .2009; 73:287-93.
59. Weiner M W, Beckett L A, Cairns N J, Green R C, Veitch D P, Aisen P S. The Alzheimer’s disease Neuroimaging Initiative: a review of papers published since its inception. Alzheimers Dement. 2012; 8: S168. 09.172.
60. Roche H M, Doyle R, Tully A M. Low serum cholesteryl ester-docosahexaenoic acid levels in Alzheimer’s disease: a case–control study. Br J Nutr. 2003; 89:483-89.
61. Morris M C, Bienias J L, Evans D A. Dietary intake of antioxidant nutrients and the risk of incidence Alzheimer disease in a biracial community study. JAMA. 2002; 287:3230-37.
62. Colacicco A M, Solfrizzi A, D’Introno A. Dietary intake of unsaturated fatty acids and age-related cognitive decline: A 8.5-year follow-up of the Italian Longitudinal Study on Aging. Neurobiol Aging. 2006; 22(6):282-286.
63. Phillips M A, Calder P C Childs C E. No Effect of Omega-3 Fatty Acid Supplementation on Cognition and Mood in Individuals with Cognitive Impairment and Probable Alzheimer's disease: A Randomised Controlled Trial. Int J Mol Sci. 2015; 16(10):24600-13.
64. Bullock R. Drug Treatments in Alzheimer Disease. Alzheimer’s disease International. Fact sheet 8. Revised April 2000. Last accessed April 1, 2004. http://www.alz.co.uk/alzheimers/treatment.html
65. Roecklein K A, Erickson K I, Miller D L. The aging hippocampus: interactions between exercise, depression, and BNDF. Neuroscientist. 2012; 18:82-97.
66. Patrick D. McGorry, Eóin Killackey, Alison Yung. Early intervention in psychosis: concepts, evidence and future directions. World Psychiatry. 2008 Oct; 7(3):148–156.
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