An insight into Alzheimer's disease and its on-setting novel genes

被引:4
作者
Vigneswaran, Jaanaky [1 ]
Muthukumar, Sivaloganathan Anogh [2 ]
Shafras, Mohamed [3 ]
Pant, Geetika [4 ]
机构
[1] Univ Mysore, Teresian Coll, Mysore, Karnataka, India
[2] Univ Mysore, Dept Studies Biochem, Mysore, Karnataka, India
[3] Sabaragamuwa Univ Sri Lanka, Fac Appl Sci, Belihuloya, Sri Lanka
[4] MS Ramaiah Coll Arts Sci & Commerce, Dept Biotechnol & Genet, Bengaluru 560054, Karnataka, India
关键词
Alzheimer's disease; Amyloid beta; ApoE; Presenilin; Mutation; Neuro-degeneration; AMYLOID PRECURSOR PROTEIN; BETA-PROTEIN; A-BETA; GAMMA-SECRETASE; RISK LOCI; TAU; MUTATION; PRESENILIN-1; CLEARANCE; MICROGLIA;
D O I
10.1186/s41983-021-00420-2
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
According to the World Health Organisation, as of 2019, globally around 50 million people suffer from dementia, with approximately another 10 million getting added to the list every year, wherein Alzheimer's disease (AD) stands responsible for almost a whopping 60-70% for the existing number of cases. Alzheimer's disease is one of the progressive, cognitive-declining, age-dependent, neurodegenerative diseases which is distinguished by histopathological symptoms, such as formation of amyloid plaque, senile plaque, neurofibrillary tangles, etc. Majorly four vital transcripts are identified in the AD complications which include Amyloid precursor protein (APP), Apolipoprotein E (ApoE), and two multi-pass transmembrane domain proteins-Presenilin 1 and 2. In addition, the formation of the abnormal filaments such as amyloid beta (A beta) and tau and their tangling with some necessary factors contributing to the formation of plaques, neuroinflammation, and apoptosis which in turn leads to the emergence of AD. Although multiple molecular mechanisms have been elucidated so far, they are still counted as hypotheses ending with neuronal death on the basal forebrain and hippocampal area which results in AD. This review article is aimed at addressing the overview of the molecular mechanisms surrounding AD and the functional forms of the genes associated with it.
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页数:16
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