Alzheimer Disease

Uzer Altaf Shaikh 1, * and Sanket P. Shinde 2

1 Delight College of Pharmacy, Koregaon Bhima, Pune, Maharashtra, India.
2 Department of Pharmaceutical Quality Assurance, Assistant Professor, Delight College of Pharmacy, Koregaon Bhima, Pune, Maharashtra, India.
 
Review
World Journal of Biology Pharmacy and Health Sciences, 2024, 18(02), 049–057.
Article DOI: 10.30574/wjbphs.2024.18.2.0239
 
Publication history: 
Received on 17 March 2024; revised on 28 April 2024; accepted on 01 May 2024
 
Abstract: 
Alzheimer's disease (AD) is typified by memory deficiencies that worsen with time, along with cognitive and behavioral abnormalities that eventually result in dementia. AD is one of the most difficult diseases to treat because of its prevalence, high cost of care, effects on patients and caregivers, and lack of mechanism-based therapies. The malfunction and loss of neurons in particular circuits and locations, especially in the populations of nerve cells supporting memory and cognition, causes the AD condition.The neuropathology of AD is characterized by intracellular and extracellular protein aggregation accumulations. In the neuronal perikarya and dystrophic neurites, abnormally phosphorylated tau forms paired helical filaments (PHFs) that combine to form neurofibrillary tangles (NFTs). The extracellular deposition of β-pleated assemblies of Aβ peptide, which result in widespread and neuritic senile plaques, is the second pathogenic hallmark.
 
Keywords: 
Alzheimer disease; Etiology; Pathogenesis; Prevention
 
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