A review on Alzheimer's disease pathophysiology and its management: an update

Kumar, Anil; Singh, Arti; Ekavali

doi:10.1016/j.pharep.2014.09.004

Cited by 1,578Alzheimer's disease research and treatmentsCholinesterase and Neurodegenerative DiseasesDementia and Cognitive Impairment Research

A review on Alzheimer's disease pathophysiology and its management: an update

Kumar, Anil, Singh, Arti, Ekavali·2015·Pharmacological Reports

DOI 10.1016/j.pharep.2014.09.004

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Abstract

Alzheimer's disease acknowledged as progressive multifarious neurodegenerative disorder, is the leading cause of dementia in late adult life. Pathologically it is characterized by intracellular neurofibrillary tangles and extracellular amyloidal protein deposits contributing to senile plaques. Over the last two decades, advances in the field of pathogenesis have inspired the researchers for the investigation of novel pharmacological therapeutics centered more towards the pathophysiological events of the disease. Currently available treatments i.e. acetylcholinesterase inhibitors (rivastigmine, galantamine, donepezil) and N-methyl d-aspartate receptor antagonist (memantine) contribute minimal impact on the disease and target late aspects of the disease. These drugs decelerate the progression of the disease, provide symptomatic relief but fail to achieve a definite cure. While the neuropathological features of Alzheimer's disease are recognized but the intricacies of the mechanism have not been clearly defined. This lack of understanding regarding the pathogenic process may be the likely reason for the non-availability of effective treatment which can prevent onset and progression of the disease. Owing to the important progress in the field of pathophysiology in the last couple of years, new therapeutic targets are available that should render the underlying disease process to be tackled directly. In this review, authors will discusses the different aspects of pathophysiological mechanisms behind Alzheimer's disease and its management through conventional drug therapy, including modern investigational therapeutic strategies, recently completed and ongoing.

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Senile amyloid plaques are formed by the extracellular nonvascular accumulation of Aβ40 and Aβ42 peptides that result from abnormal processing of amyloid precursor protein by the β- and γ-secretases and an imbalance in production and clearance pathways.
“Senile amyloid plaques or “miliary foci” as described by Alzheimer in the description of Alzheimer’s disease and originally that same year by Oskar Fischer are formed by the extracellular nonvascular accumulation of Aβ40 and Aβ42 peptides that result from the abnormal processing of amyloid precursor protein by the β- and γ-secretases and an imbalance in the production and clearance pathways [1, 27”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [27]
Cholinesterase inhibitors and memantine only temporarily relieve symptoms of AD patients but do not delay progression of the disease.
“These cholinesterase inhibitors and NMDA receptor antagonist memantine only temporarily relieve the symptoms of AD patients but do not delay the progression of the disease [206, 207].”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [207]
Amyloid-β plaques and Tau protein hyper-phosphorylation are considered hallmarks of Alzheimer disease.
“Amyloid-β plaques and Tau protein hyper-phosphorylation are considered as hallmarks of AD”
From Nanotechnology: A Promising Approach for Delivery of Neuroprotective Drugs (2020) · cites this paper as Kumar and Singh, 2015

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Background
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Authors: Kumar, A., Singh, A., & Ekavali
Affiliations: Panjab University (IN)
Corresponding author: Kumar, Anil
ORCID: Kumar, Anil
Singh, Arti
Venue: Pharmacological Reports
Publisher: Springer Science and Business Media LLC
Published: 2015-04
Volume: 67
Issue: 2
Pages: 195-203
ISSN: 1734-1140 (ISSN-L)
DOI: 10.1016/j.pharep.2014.09.004
OpenAlex: W2049771698
Cited by: 1,578
References: 115
Citations by year: 2026: 61 · 2025: 102 · 2024: 155 · 2023: 160 · 2022: 176 · 2021: 185 · 2020: 176 · 2019: 199 · 2018: 136 · 2017: 118 · 2016: 80 · 2015: 28 · 2014: 1
FWCI: 8.97
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Pharmacological Reports (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Health Sciences › Medicine › Pharmacology › Cholinesterase and Neurodegenerative Diseases
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords: Alzheimer's disease, pathophysiology, neurofibrillary tangles, amyloid plaques, acetylcholinesterase inhibitors, memantine, NMDA receptor antagonists, symptomatic treatment, disease-modifying therapy, therapeutic target, dementia
MeSH terms: Alzheimer Disease, Cholinesterase Inhibitors, Humans, Inflammation, Memantine, Mitochondria, Synaptic Transmission, Signal Transduction, Drugs, Investigational, Amyloid beta-Peptides, tau Proteins, Oxidative Stress, Molecular Targeted Therapy

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A review on Alzheimer's disease pathophysiology and its management: an update

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