Neuropathology and therapeutic management of Alzheimer's disease - an update

  • Kumar A
  • Dogra S
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A review. Alzheimer's disease (AD) is a progressive neurodegenerative disorder which is the principal cause of dementia throughout the world and the fourth cause of death in developed countries. The pathol. hallmarks of this disease are regionalized neuronal dysfunction/death, accumulation of senile plaques extracellularly and neurofibrillary tangles (NFTs) intraneuronally. Several hypotheses have been put forth to explain the pathophysiol. of this disease, including aberrant b-amyloid (Ab) metab., hyperphosphorylation of cytoskeletal proteins, genetic predisposition (mutations in genes coding for presenilin-1 and -2 (PS-1 and PS-2) and amyloid precursor protein (APP), apolipoprotein E genotype, oxidative stress, excitotoxicity, inflammation and abnormal cell cycle re-entry. However, none of these hypotheses alone is sufficient to explain the diversity of biochem. and pathol. abnormalities in AD. Currently, medications approved by the United States FDA for AD include acetylcholinesterase (AChE) inhibitors and memantine. However, these drugs provide only symptomatic relief and do not stop disease progression. The major focus of research now is to find novel therapeutic drug candidates targeting the underlying pathophysiol. mechanisms. These therapeutic strategies include drugs targeting amyloid and tau pathol., immunotherapy, neurotransmitter replacement therapy, nutraceuticals and disease-modifying therapies. The main focus of this review is to provide new insight on the various mechanisms involved in the neuropathol. of AD and shed light on current and future treatment strategies aimed at improving both cognitive deficits and halting the deadly neurodegenerative progression of the disease. [on SciFinder (R)]

Author-supplied keywords

  • AD
  • APP
  • Alzheimer
  • Alzheimer's disease
  • Apolipoprotein E
  • Cognition
  • Dementia
  • Immunotherapy
  • Neurofibrillary tangles
  • Neurotoxicity
  • PS1
  • Treatment strategies
  • amyloid
  • amyloid precursor protein
  • gene
  • hyperphosphorylation
  • inflammation
  • inhibitor
  • memantine
  • mutation
  • neurofibrillary tangle
  • oxidative stress
  • phosphorylation
  • plaques
  • presenilin
  • presenilin 1
  • presenilin1
  • review
  • senile plaques
  • tangles
  • tau

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  • Anil Kumar

  • Samrita Dogra

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