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Amyloidogenesis in Alzheimer's disease: some possible therapeutic opportunities

S Gandy1, P Greengard

  • 1Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, New York 10021.

Trends in Pharmacological Sciences
|March 1, 1992
PubMed

Insights

Alzheimer's disease is linked to beta/A4 amyloid protein fibrils in the brain. Research explores amyloid precursor protein (APP) gene mutations and therapeutic targets for this neurodegenerative condition.

Area of Science:

  • Neuroscience
  • Genetics
  • Biochemistry

Background:

  • Alzheimer's disease is characterized by cerebral amyloid plaques.
  • Beta/A4 amyloid protein fibril deposition is a hallmark of Alzheimer's disease.
  • Mutations in the amyloid precursor protein (APP) gene are linked to familial forms of the disease.

Purpose of the Study:

  • To review recent studies on cerebral amyloidosis.
  • To elucidate the cell biology of amyloidogenesis.
  • To discuss potential therapeutic strategies for Alzheimer's disease.

Main Methods:

  • Review of existing literature on Alzheimer's disease and amyloidogenesis.
  • Analysis of genetic studies involving APP gene mutations.
  • Examination of cellular mechanisms, including protein phosphorylation, affecting APP processing.

Main Results:

  • Cerebral amyloid deposition is a consistent feature of Alzheimer's disease.
  • APP gene mutations are associated with familial cerebral amyloidoses.
  • Protein phosphorylation significantly influences APP expression and processing.

Conclusions:

  • Understanding amyloidogenesis is crucial for Alzheimer's disease research.
  • Targeting APP processing pathways may offer therapeutic avenues.
  • Further research into cell biology and genetics can guide treatment development.

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