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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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Characterizing dysregulations via cell-cell communications in Alzheimer's brains using single-cell transcriptomes.

Che Yu Lee1, Dylan Riffle1, Yifeng Xiong1

  • 1Department of Computer Science, University of California, Irvine, CA, USA.

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Summary

Alzheimer's disease disrupts brain cell communication, altering signaling pathways and linking risk genes. This study reveals cell-type-specific communication changes in AD, offering a mechanistic view of the disease.

Keywords:
Alzheimer’s DiseaseBrainCell-cell communicationLigand-receptorNetworkSingle-nucleus RNA-seq

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Area of Science:

  • Neuroscience
  • Genomics
  • Cell Biology

Background:

  • Alzheimer's disease (AD) affects 44 million globally, causing cognitive decline.
  • Single-cell sequencing offers high-resolution gene expression analysis.
  • Understanding cell-to-cell communication in the brain's microenvironment is crucial for AD research.

Purpose of the Study:

  • Investigate cell-to-cell communication networks in the human prefrontal cortex.
  • Compare communication patterns in healthy brains versus Alzheimer's disease (AD) brains.
  • Identify specific signaling pathway dysregulations and their links to AD risk genes.

Main Methods:

  • Utilized large-scale, single-nucleus RNA sequencing (snRNA-seq) data from the human prefrontal cortex.
  • Processed snRNA-seq data with strict quality controls and cell type annotation.
  • Constructed a cell-to-cell communication network using ligand and receptor gene expression.

Main Results:

  • Normal brains show overlapping signaling networks between related cell types; AD brains exhibit mixed cell types and signaling.
  • Excitatory neurons in AD increase communication with inhibitory neurons; other cells decrease communication.
  • Canonical pathways (CSF, TGFβ, CX3C) are dysregulated in AD, particularly involving microglia/PVM and endothelial-to-neuronal signaling (WNT pathway).
  • Extracellular AD risk genes (APP, APOE, PSEN1) connect to intracellular risk genes (TREM2, ABCA1, APP) in astrocyte/microglia-to-neuron communication.

Conclusions:

  • Cellular signaling in AD is regulated in a cell-type-specific manner.
  • Dysregulation of extracellular signaling genes is linked to intracellular AD risk genes.
  • This study provides a mechanistic, intra- and inter-cellular perspective on Alzheimer's disease.