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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...
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: 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...
Long-term Depression01:03

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
If over time, all...

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Related Experiment Video

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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

Synaptic dysfunction in Alzheimer's disease.

Elena Marcello1, Roberta Epis, Claudia Saraceno

  • 1Department of Pharmacological Sciences and Centre of Excellence on Neurodegenerative Diseases, University of Milan, Via Balzaretti 9, 20133 Milan, Italy. elena.marcello@unimi.it

Advances in Experimental Medicine and Biology
|February 22, 2012
PubMed
Summary
This summary is machine-generated.

Alzheimer's disease (AD) involves amyloid peptide (Aβ) generation. Soluble Aβ assemblies disrupt synaptic function, causing cognitive deficits, with mechanisms still under investigation.

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Published on: July 14, 2010

Area of Science:

  • Neuroscience
  • Biochemistry
  • Pathology

Background:

  • Alzheimer's disease (AD) pathogenesis is initiated by amyloid peptide (Aβ) generation.
  • Amyloid precursor protein (APP) processing by β- and γ-secretases produces Aβ.
  • α-secretase cleavage of APP inhibits Aβ deposition.

Purpose of the Study:

  • Investigate the role of soluble Aβ assemblies in synaptic dysfunction and cognitive deficits.
  • Identify Aβ oligomer targets and cellular mechanisms underlying Aβ-induced synaptic failure.

Main Methods:

  • Analysis of Aβ production pathways involving APP, β-secretase, and γ-secretase.
  • Examination of α-secretase's role in preventing Aβ deposition.
  • Research into soluble Aβ assemblies and their impact on synaptic function.

Main Results:

  • Soluble Aβ assemblies can cause cognitive impairment by disrupting synaptic function.
  • A toxic gain-of-function mechanism involves Aβ self-association and novel interactions impairing plasticity.
  • Aβ may have a physiological role; insufficient or excess Aβ can precipitate dysfunction.

Conclusions:

  • Soluble Aβ assemblies are key contributors to Alzheimer's disease-related cognitive deficits.
  • Understanding Aβ's physiological role and synaptic targets is crucial for future AD research.
  • Further research is needed to fully elucidate the mechanisms of Aβ-induced synaptic dysfunction.