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Alzheimer's disease: pathogenesis, diagnostics, and therapeutics

International journal of nanomedicine, , Vol.14, p.5541-5554 [Peer Reviewed Journal]

COPYRIGHT 2019 Dove Medical Press Limited ;2019. This work is licensed under https://creativecommons.org/licenses/by-nc/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2019 Tiwari et al. 2019 Tiwari et al. ;ISSN: 1178-2013 ;ISSN: 1176-9114 ;EISSN: 1178-2013 ;DOI: 10.2147/ijn.s200490 ;PMID: 31410002

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Title:
Alzheimer's disease: pathogenesis, diagnostics, and therapeutics
Author: Tiwari, Sneham ; Atluri, Venkata ; Kaushik, Ajeet ; Yndart, Adriana ; Nair, Madhavan
Subjects: Advertising executives ; Aggregates ; Alzheimer Disease - diagnosis ; Alzheimer Disease - genetics ; Alzheimer Disease - pathology ; Alzheimer Disease - therapy ; Alzheimer's disease ; Alzheimers disease ; Amyloid Beta Amyloidogenesis Amyloid precursor proteins β-secretase gamma-secretase Tau phosphorylation ; Amyloid beta-Peptides - chemistry ; Amyloid beta-Peptides - metabolism ; Amyloidosis ; Blood-Brain Barrier - pathology ; Brain ; Brain research ; Central nervous system ; Dementia ; Development and progression ; Drugs ; Epigenesis, Genetic ; HIV ; Human immunodeficiency virus ; Humans ; Mutation ; Nanoparticles ; Nanotechnology ; Nervous system ; Neurophysiology ; Pathogenesis ; Peptides ; Plaque, Amyloid - pathology ; Polymerization ; Precision medicine ; Proteins ; Review ; Therapeutics
Is Part Of: International journal of nanomedicine, , Vol.14, p.5541-5554
Description: Currently, 47 million people live with dementia globally, and it is estimated to increase more than threefold (~131 million) by 2050. Alzheimer's disease (AD) is one of the major causative factors to induce progressive dementia. AD is a neurodegenerative disease, and its pathogenesis has been attributed to extracellular aggregates of amyloid β (Aβ) plaques and intracellular neurofibrillary tangles made of hyperphosphorylated τ-protein in cortical and limbic areas of the human brain. It is characterized by memory loss and progressive neurocognitive dysfunction. The anomalous processing of APP by β-secretases and γ-secretases leads to production of Aβ and Aβ monomers, which further oligomerize and aggregate into senile plaques. The disease also intensifies through infectious agents like HIV. Additionally, during disease pathogenesis, the presence of high concentrations of Aβ peptides in central nervous system initiates microglial infiltration. Upon coming into vicinity of Aβ, microglia get activated, endocytose Aβ, and contribute toward their clearance via TREM2 surface receptors, simultaneously triggering innate immunoresponse against the aggregation. In addition to a detailed report on causative factors leading to AD, the present review also discusses the current state of the art in AD therapeutics and diagnostics, including labeling and imaging techniques employed as contrast agents for better visualization and sensing of the plaques. The review also points to an urgent need for nanotechnology as an efficient therapeutic strategy to increase the bioavailability of drugs in the central nervous system.
Publisher: New Zealand: Dove Medical Press Limited
Language: English
Identifier: ISSN: 1178-2013
ISSN: 1176-9114
EISSN: 1178-2013
DOI: 10.2147/ijn.s200490
PMID: 31410002
Source: Open Access: DOAJ Directory of Open Access Journals
Open Access: PubMed Central
Geneva Foundation Free Medical Journals at publisher websites
AUTh Library subscriptions: ProQuest Central
MEDLINE
Dove Press Free

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Alzheimer's disease: pathogenesis, diagnostics, and therapeutics

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