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Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...

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A Novel In Vitro Live-imaging Assay of Astrocyte-mediated Phagocytosis Using pH Indicator-conjugated Synaptosomes
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Attenuating astrocyte activation accelerates plaque pathogenesis in APP/PS1 mice.

Andrew W Kraft1, Xiaoyan Hu, Hyejin Yoon

  • 1The Hope Center for Neurological Disorders, Knight Alzheimer's Disease Research Center, Department of Neurology, Washington University School of Medicine, St. Louis, Missouri 63124, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|October 6, 2012
PubMed
Summary

Astrocyte activation, involving glial fibrillary acid protein (GFAP) and vimentin (VIM), limits Alzheimer's disease plaque growth and reduces neurite damage. Deleting these proteins in mice paradoxically increased amyloid plaque accumulation.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Pathology

Background:

  • Alzheimer's disease (AD) is characterized by amyloid-beta (Aβ) plaques.
  • Reactive astrocytes surround amyloid plaques, but their role in AD pathogenesis is unknown.

Purpose of the Study:

  • To investigate the role of astrocyte activation in Alzheimer's disease pathogenesis.
  • To determine if glial fibrillary acid protein (GFAP) and vimentin (VIM) are essential for astrocyte-mediated control of amyloid plaque accumulation and associated neuropathology.

Main Methods:

  • Generated transgenic mice lacking GFAP and VIM genes (Gfap(-/-)Vim(-/-)) expressing mutant amyloid precursor protein and presenilin-1 (APP/PS1).
  • Quantified amyloid plaque load, Aβ levels, and astrocyte morphology in APP/PS1 Gfap(-/-)Vim(-/-) mice compared to controls (APP/PS1 Gfap(+/+)Vim(+/+)).
  • Assessed the presence and severity of dystrophic neurites in relation to amyloid plaques.

Main Results:

  • Deletion of GFAP and VIM genes in APP/PS1 mice resulted in a twofold increase in amyloid plaque load at 8 and 12 months of age.
  • Aβ generation and processing remained unaffected by GFAP/VIM gene deletion.
  • Gfap(-/-)Vim(-/-) astrocytes exhibited reduced process hypertrophy and lacked intimate contact with amyloid plaques, correlating with a 2- to 3-fold increase in dystrophic neurites.

Conclusions:

  • Astrocyte activation, mediated by GFAP and VIM, plays a crucial role in limiting amyloid plaque growth in Alzheimer's disease models.
  • Astrocyte-plaque interaction is essential for attenuating the formation of dystrophic neurites, a key neuropathological feature of AD.
  • Targeting astrocyte activation pathways could offer a novel therapeutic strategy for Alzheimer's disease.