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Related Concept Videos

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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Related Experiment Video

Updated: May 21, 2026

Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease
06:52

Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease

Published on: July 6, 2019

Synaptic changes in Alzheimer's disease and its models.

J Pozueta1, R Lefort, M L Shelanski

  • 1Taub Institute for Research on Alzheimer's Disease and the Aging Brain and Department of Pathology and Cell Biology, Columbia University, New York, NY 10032, United States.

Neuroscience
|June 13, 2012
PubMed
Summary

Soluble amyloid-beta (Aβ) oligomers, not just fibrils, are key drivers of Alzheimer's disease (AD) cognitive decline by targeting synapses. Understanding these Aβ oligomer effects is crucial for developing effective AD therapies.

Keywords:
(11)C-labeled Pittsburg compound BADADDLAPPAlzheimer’s diseaseAβ-derived diffusible ligandCREBEOFADFrizzledFzGAPGEFGTPase activating proteinsLTDLTPN-methyl-d-aspartateNFTNMDANMDARPAKPDAPPPiBPrPCSPamyloid precursor proteinbeta-amyloidcAMP response element binding proteincellular prion proteindendritic spinesearly-onset familial ADguanine nucleotide exchange factorlearning and memorylong-term depressionlong-term potentiationmTORmTOR complex 2mTORC2mammalian target of rapamycinmouse modelneurofibrillary tangleneuron-specific promoterp21-activated kinasesenile plaquesynapse

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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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Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons
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Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons

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Last Updated: May 21, 2026

Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease
06:52

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Published on: July 6, 2019

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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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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Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons
06:23

Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons

Published on: October 30, 2018

Area of Science:

  • Neuroscience
  • Pathology
  • Biochemistry

Background:

  • Alzheimer's disease (AD) is a prevalent neurodegenerative disorder marked by cognitive decline.
  • Hallmark lesions include senile plaques (SP) and neurofibrillary tangles (NFT).
  • Initially, fibrillar amyloid-beta (Aβ) was considered the primary cause of neurodegeneration.

Purpose of the Study:

  • To review evidence supporting the Aβ oligomer-centric hypothesis in AD.
  • To explore the effects of Aβ oligomers on synapses.
  • To provide a framework for AD research and therapeutic development.

Main Methods:

  • Literature review of studies on Aβ oligomers and synaptic function.
  • Analysis of evidence linking Aβ oligomers to cognitive deficits.
  • Examination of morphological and functional synaptic changes induced by Aβ oligomers.

Main Results:

  • Soluble Aβ oligomers, rather than fibrils, are implicated in triggering cognitive deficits.
  • Aβ oligomers specifically target synapses and disrupt synaptic signaling pathways.
  • Evidence supports a shift in understanding AD pathogenesis towards soluble Aβ forms.

Conclusions:

  • The Aβ oligomer-centric hypothesis is increasingly accepted in AD research.
  • Understanding Aβ oligomer-synapse interactions is vital for therapeutic strategies.
  • Targeting Aβ oligomers may offer a pathway to alter or reverse AD progression.