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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...
Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining, normally used to...
Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining, normally used to...
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
Dementia l: Introduction01:22

Dementia l: Introduction

Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...

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Related Experiment Video

Updated: Jun 20, 2026

Preparation of Oligomeric &beta;-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices
04:41

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

Published on: July 14, 2010

Alzheimer's disease amyloid beta-protein and synaptic function.

Tomas Ondrejcak1, Igor Klyubin, Neng-Wei Hu

  • 1Department of Pharmacology and Therapeutics, Biotechnology Building and Institute of Neuroscience, Trinity College, Dublin 2, Ireland.

Neuromolecular Medicine
|September 17, 2009
PubMed
Summary

Soluble amyloid beta disrupts synaptic plasticity in Alzheimer's disease (AD) by affecting glutamatergic and cholinergic systems. Targeting these neurotransmitter pathways may offer new therapeutic strategies for AD.

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Area of Science:

  • Neuroscience
  • Pathophysiology
  • Molecular Biology

Background:

  • Alzheimer's disease (AD) is characterized by amyloid beta-protein (A beta) deposition, with soluble A beta species correlating with dementia severity.
  • Synaptic loss in the brain is the primary correlate of cognitive impairment in AD.
  • Research focuses on how soluble A beta disrupts synaptic mechanisms in vulnerable brain regions like the hippocampus.

Purpose of the Study:

  • To review the involvement of neurotransmitter intercellular signaling in mediating or modulating the synaptic plasticity-disrupting actions of soluble A beta.
  • To emphasize the roles of glutamatergic and cholinergic mechanisms in AD pathophysiology.
  • To inform future clinical trials for AD therapeutics.

Main Methods:

  • Review of existing literature on Alzheimer's disease, amyloid beta, synaptic plasticity, and neurotransmitter signaling.
  • Analysis of studies investigating the effects of soluble A beta on synaptic plasticity in the hippocampus.
  • Examination of the roles of NMDA, nicotinic, and muscarinic receptors in mediating A beta's actions.

Main Results:

  • Soluble A beta potently and selectively disrupts synaptic plasticity, inhibiting long-term potentiation (LTP) and enhancing long-term depression (LTD) of glutamatergic transmission.
  • These actions of A beta contribute to reduced synaptic integrity over time.
  • NMDA and possibly nicotinic receptors are critically involved in mediating A beta's disruptive effects.

Conclusions:

  • Neurotransmitter signaling, particularly glutamatergic and cholinergic mechanisms, plays a key role in how soluble A beta disrupts synaptic plasticity.
  • Targeting muscarinic receptors may indirectly modulate A beta's actions.
  • Understanding these mechanisms can guide the development of drugs targeting glutamatergic and cholinergic systems for Alzheimer's disease treatment.