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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...
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...
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...
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...
Chemical Synapses01:26

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Chemical Synapses01:26

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...

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Related Experiment Video

Updated: May 23, 2026

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices
07:44

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

Published on: October 6, 2017

Synapses and Alzheimer's disease.

Morgan Sheng1, Bernardo L Sabatini, Thomas C Südhof

  • 1Department of Neuroscience, Genentech Inc., South San Francisco, California 94080, USA. sheng.morgan@gene.com

Cold Spring Harbor Perspectives in Biology
|April 12, 2012
PubMed
Summary

Alzheimer's disease (AD) involves amyloid-beta plaques and tau tangles. Research shows oligomeric Aβ species harm synapses, while reduced presenilin function impairs brain function and promotes neurodegeneration.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Genetics

Background:

  • Alzheimer's disease (AD) is a leading cause of dementia in older adults.
  • Pathology involves amyloid-beta (Aβ) plaques and hyperphosphorylated tau tangles.
  • Familial AD linked to increased Aβ production or altered presenilin activity.

Purpose of the Study:

  • To explore key themes in Alzheimer's disease pathogenesis.
  • To investigate the detrimental effects of oligomeric Aβ species on synapses.
  • To examine the impact of decreased presenilin function on synaptic transmission and neurodegeneration.

Main Methods:

  • Analysis of Aβ-peptide aggregation and amyloid precursor protein processing.
  • Investigation of tau protein hyperphosphorylation and filament formation.

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A Novel In Vitro Live-imaging Assay of Astrocyte-mediated Phagocytosis Using pH Indicator-conjugated Synaptosomes
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A Novel In Vitro Live-imaging Assay of Astrocyte-mediated Phagocytosis Using pH Indicator-conjugated Synaptosomes

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  • Studies on synaptic function, structure, and transmission in relation to Aβ and presenilin activity.

    • Main Results:

    • Oligomeric Aβ species significantly impair synapse function and structure, particularly postsynaptically.
    • Reduced presenilin function leads to impaired synaptic transmission and promotes neurodegeneration.
    • Mechanisms underlying these processes are being elucidated.

    Conclusions:

    • Oligomeric Aβ and impaired presenilin function are critical factors in Alzheimer's disease pathogenesis.
    • Understanding these mechanisms may reveal new therapeutic strategies for AD.
    • Further research is needed to fully elucidate the relevance of these findings to AD.