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Aß Pathology and Neuron-Glia Interactions: A Synaptocentric View.

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Alzheimer's disease (AD) is a synaptic disease. Amyloid-ß (Aß) accumulation impairs neurons, astrocytes, and microglia, disrupting the quad-partite synapse and leading to dementia.

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Area of Science:

  • Neuroscience
  • Neuropathology
  • Cellular Biology

Background:

  • Alzheimer's disease (AD) is the leading cause of dementia globally.
  • Key early AD pathologies include amyloid-ß (Aß) accumulation and glial cell activation (astrocytes and microglia).
  • The synapse, particularly the quad-partite synapse (neurons, astrocytes, microglia), is increasingly recognized as central to AD pathogenesis.

Purpose of the Study:

  • To review how amyloid-ß (Aß) accumulation functionally impacts the components of the quad-partite synapse in Alzheimer's disease.
  • To highlight the effects of Aß on synaptic processes, astrocyte functions, and microglial roles.

Main Methods:

  • Literature review of current knowledge on Aß effects on synaptic components.
  • Analysis of studies focusing on presynaptic and postsynaptic neuronal function.
  • Examination of research on astrocyte neurotransmitter recycling, gliotransmission, and ion homeostasis.
  • Review of literature on Aß-induced changes in microglial immunoprotective functions.

Main Results:

  • Amyloid-ß (Aß) accumulation progressively deteriorates pre- and postsynaptic neuronal functions.
  • Aß disrupts astrocyte functions, including neurotransmitter recycling, gliotransmission, and ion homeostasis.
  • Aß alters the immunoprotective roles of microglia during Alzheimer's disease progression.

Conclusions:

  • Alzheimer's disease is fundamentally a disease of the quad-partite synapse, driven by Aß.
  • Understanding Aß's impact on each synaptic component is crucial for developing effective AD therapies.
  • Further research is needed to address current challenges and advance AD therapeutic strategies.