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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...
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...
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's Disease: Treatment01:22

Alzheimer's Disease: Treatment

Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
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 29, 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

Alzheimer's disease: synapses gone cold.

Robert M Koffie1, Bradley T Hyman, Tara L Spires-Jones

  • 1Massachusetts General Hospital, Harvard Medical School, 114 16th Street, Charlestown, MA 02129, USA. tspires@partners.org.

Molecular Neurodegeneration
|August 30, 2011
PubMed
Summary

Alzheimer's disease (AD) involves synapse loss, with amyloid beta (Aβ) oligomers harming neuronal connections. Understanding Aβ's impact on synapses offers potential therapeutic targets for AD.

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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 &#946; Effects in Cultured Mouse Neurons
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Last Updated: May 29, 2026

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices
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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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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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Area of Science:

  • Neuroscience
  • Pathology
  • Biochemistry

Background:

  • Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by cognitive decline.
  • Synapse loss is a key pathological feature correlating with cognitive impairment in AD.
  • Evidence indicates AD is fundamentally a disease of synaptic dysfunction.

Purpose of the Study:

  • To review recent findings on Alzheimer's disease pathogenesis.
  • To focus on the impact of amyloid beta (Aβ) on synapses.
  • To elucidate molecular underpinnings for potential therapeutic targets.

Main Methods:

  • Review of in vitro and in vivo studies on Aβ oligomer toxicity.
  • Analysis of electrophysiological data (LTP/LTD) related to Aβ.
  • Examination of animal models demonstrating Aβ-induced synapse loss and cognitive impairment.

Main Results:

  • Soluble oligomeric forms of amyloid beta (Aβ) are toxic to neuronal synapses.
  • Aβ oligomers inhibit long-term potentiation (LTP) and facilitate long-term depression (LTD).
  • Oligomeric Aβ induces synapse loss and cognitive impairment in animal models.

Conclusions:

  • Aβ oligomers play a critical role in Alzheimer's disease pathogenesis by disrupting synaptic function.
  • Understanding the molecular mechanisms of Aβ-synapse interactions is crucial for developing effective AD treatments.
  • Targeting Aβ's effects on synapses presents a promising therapeutic strategy for Alzheimer's disease.