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

Abstract 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 numbe...

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Autores principales:	Jaanaky Vigneswaran, Sivaloganathan Anogh Muthukumar, Mohamed Shafras, Geetika Pant
Formato:	article
Lenguaje:	EN
Publicado:	SpringerOpen 2021
Materias:	Alzheimer’s disease Amyloid beta ApoE Presenilin Mutation Neuro-degeneration Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571
Acceso en línea:	https://doaj.org/article/0c07c571fb1f4ffbaf77383bdb11835d
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spelling	oai:doaj.org-article:0c07c571fb1f4ffbaf77383bdb11835d2021-12-05T12:10:06ZAn insight into Alzheimer’s disease and its on-setting novel genes10.1186/s41983-021-00420-21687-8329https://doaj.org/article/0c07c571fb1f4ffbaf77383bdb11835d2021-11-01T00:00:00Zhttps://doi.org/10.1186/s41983-021-00420-2https://doaj.org/toc/1687-8329Abstract 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 (Aβ) 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.Jaanaky VigneswaranSivaloganathan Anogh MuthukumarMohamed ShafrasGeetika PantSpringerOpenarticleAlzheimer’s diseaseAmyloid betaApoEPresenilinMutationNeuro-degenerationNeurosciences. Biological psychiatry. NeuropsychiatryRC321-571ENThe Egyptian Journal of Neurology, Psychiatry and Neurosurgery, Vol 57, Iss 1, Pp 1-16 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Alzheimer’s disease Amyloid beta ApoE Presenilin Mutation Neuro-degeneration Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571
spellingShingle	Alzheimer’s disease Amyloid beta ApoE Presenilin Mutation Neuro-degeneration Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Jaanaky Vigneswaran Sivaloganathan Anogh Muthukumar Mohamed Shafras Geetika Pant An insight into Alzheimer’s disease and its on-setting novel genes
description	Abstract 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 (Aβ) 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.
format	article
author	Jaanaky Vigneswaran Sivaloganathan Anogh Muthukumar Mohamed Shafras Geetika Pant
author_facet	Jaanaky Vigneswaran Sivaloganathan Anogh Muthukumar Mohamed Shafras Geetika Pant
author_sort	Jaanaky Vigneswaran
title	An insight into Alzheimer’s disease and its on-setting novel genes
title_short	An insight into Alzheimer’s disease and its on-setting novel genes
title_full	An insight into Alzheimer’s disease and its on-setting novel genes
title_fullStr	An insight into Alzheimer’s disease and its on-setting novel genes
title_full_unstemmed	An insight into Alzheimer’s disease and its on-setting novel genes
title_sort	insight into alzheimer’s disease and its on-setting novel genes
publisher	SpringerOpen
publishDate	2021
url	https://doaj.org/article/0c07c571fb1f4ffbaf77383bdb11835d
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An insight into Alzheimer’s disease and its on-setting novel genes

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