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Related Concept Videos

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Related Experiment Video

Updated: May 15, 2025

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
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SFRP1 upregulation causes hippocampal synaptic dysfunction and memory impairment.

Guadalupe Pereyra1, María Inés Mateo1, Pablo Miaja1

  • 1Centro de Biología Molecular Severo Ochoa, CSIC-UAM, Campus de la Universidad Autónoma de Madrid, 28049 Madrid, Spain; CIBER de Enfermedades Raras (CIBERER), 28029 Madrid, Spain.

Cell Reports
|April 8, 2025
PubMed
Summary
This summary is machine-generated.

Elevated SFRP1 in Alzheimer's disease (AD) impairs neuronal function, causing early synaptic defects and cognitive decline. This highlights glial factors in AD pathogenesis and suggests a mechanism for synaptopathy in prodromal AD.

Keywords:
ADAM10Alzheimer’s diseaseCP: Neuroscienceastrocytesdendritic spinesmicroglianeurexinneurodegenerationproteomicsstructural synaptic moleculessynaptic plasticity

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Area of Science:

  • Neuroscience
  • Neurodegenerative Diseases
  • Molecular Biology

Background:

  • Impaired neuronal and synaptic function characterize early Alzheimer's disease (AD), preceding other pathological changes and cognitive deficits.
  • Glial-derived protein SFRP1 is elevated in AD brains from preclinical stages and contributes to disease progression.
  • Glial factors are implicated in the early pathogenesis of Alzheimer's disease.

Purpose of the Study:

  • To investigate the role of astrocytic SFRP1 in Alzheimer's disease pathogenesis.
  • To determine the effects of SFRP1 overexpression on neuronal and synaptic function.
  • To elucidate the molecular mechanisms linking SFRP1 to synaptic dysfunction and cognitive decline in a mouse model.

Main Methods:

  • Generation and analysis of transgenic mice overexpressing astrocytic SFRP1.
  • Assessment of dendritic and synaptic morphology, synaptic plasticity (long-term potentiation), and cognitive function.
  • Proteomic analysis to identify molecular changes associated with SFRP1 accumulation.
  • Immunohistochemistry and co-localization studies in cultured hippocampal neurons.

Main Results:

  • Overexpression of astrocytic SFRP1 led to early dendritic and synaptic defects in adult mice.
  • Impaired synaptic long-term potentiation and cognitive decline were observed in aged SFRP1-overexpressing mice.
  • Proteomic analysis revealed increased levels of structural synaptic proteins, such as neurexin, correlating with SFRP1 accumulation.
  • SFRP1 was found in close proximity to neurexin in cultured hippocampal neurons.

Conclusions:

  • Excessive SFRP1 hinders synaptic protein turnover, leading to reduced synaptic plasticity.
  • This mechanism may underlie the synaptopathy observed in the brains of prodromal Alzheimer's disease patients.
  • Astrocytic SFRP1 plays a critical role in early AD pathogenesis by disrupting synaptic function.