Affiliation:
1. Chitkara College of Pharmacy, Chitkara University, Punjab, India
Abstract
Abstract:
Alzheimer's disease (AD) is a psychological, biological, or developmental
disorder that affects basic mental functioning. AD is generally affiliated with marked
discomfort and impaired social, professional, or other crucial aspects of life. AD is
predominant worldwide, but a disparity in prevalence is observed amongst nations.
Around 3/4 of people with Alzheimer's disease are from underdeveloped nations, which
receive only 1/10th of global mental health resources. Residents of each community and
age category share their presence in the overall load of AD. AD is a multifactorial
disease impacted by numerous environmental, genetic, and endogenous elements.
Heteromorphic interactive downstream cascades, networks, and molecular mechanisms
(inflammation and immune network, cholinergic deficit, lipid transit, endocytosis,
excitotoxicity, oxidative stress, amyloid and tau pathology, energy metabolism, neuron
and synapse loss, and cell death) have been isolated, imparting a non-dissociative
contribution in pathogenesis of AD. In the CNS, the structural organization of cholinergic
neurons can give a novel insight into the mechanism of new learning. The alleviation of
central cholinergic transposal following destruction in the basal forebrain cholinergic
neurons precipitates a decline in neurocognitive symptoms visible in AD patients. The
brain of patients suffering from AD exhibits plaques of aggregated amyloid-β and
neurofibrillary tangles containing hyperphosphorylated tau protein. Amyloid-β triggers
cholinergic loss by modulation of calcium and generation of cell-damaging molecules
such as nitric oxide and reactive oxygen species intermediates. The present review
focuses on the pathogenic mechanisms related to stages, diagnosis, and therapeutic
approaches involved in AD.
Publisher
Bentham Science Publishers Ltd.
Subject
Molecular Biology,Molecular Medicine,General Medicine,Biochemistry
Cited by
8 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献