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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...
Dementia01:30

Dementia

Dementia is a collective term for cognitive disorders primarily affecting memory, thinking, and reasoning. It is not a specific disease but a syndrome, with Alzheimer's disease being the most common cause, accounting for approximately 60-80% of cases. Other types include vascular dementia, Lewy body dementia, and frontotemporal dementia. Dementia affects millions worldwide, particularly older adults, though it is not a normal part of aging.
The progression of dementia is generally gradual.

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Related Experiment Video

Updated: Jun 10, 2026

Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits
08:01

Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits

Published on: March 16, 2016

Plasma ß-amyloid and cognitive decline.

Stephanie A Cosentino1, Yaakov Stern, Elisaveta Sokolov

  • 1The Gertrude H. Sergievsky Center, Taub Institute for Research in Alzheimer’s Disease and the Aging Brain, Columbia University Medical Center, New York, NY 10032, USA.

Archives of Neurology
|August 11, 2010
PubMed
Summary

Plasma beta-amyloid (Aβ) levels correlate with cognitive decline, particularly memory loss, in individuals who may or may not develop Alzheimer disease (AD). Higher Aβ levels and decreasing Aβ42 are linked to faster cognitive changes.

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

Published on: July 14, 2010

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Last Updated: Jun 10, 2026

Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits
08:01

Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits

Published on: March 16, 2016

Preparation of Oligomeric β-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

Area of Science:

  • Neurology
  • Biochemistry
  • Gerontology

Background:

  • Alzheimer disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline.
  • Plasma biomarkers, such as beta-amyloid (Aβ), are being investigated for their potential role in early AD detection and prediction.
  • Understanding the relationship between plasma Aβ levels and cognitive changes is crucial for identifying individuals at risk for AD.

Purpose of the Study:

  • To investigate the association between plasma β-amyloid (Aβ) levels and cognitive changes.
  • To determine if plasma Aβ levels predict conversion to Alzheimer disease (AD).
  • To examine the relationship between plasma Aβ levels and cognitive decline independent of dementia.

Main Methods:

  • A longitudinal study was conducted over approximately 4.5 years with 3 visits.
  • Participants included 880 individuals from a diverse community sample, free of dementia at baseline, with two plasma Aβ measurements.
  • General estimating equations were used to analyze the association between plasma Aβ levels and cognitive changes.

Main Results:

  • High baseline plasma Aβ42 and Aβ40, along with decreasing/stable Aβ42, were associated with faster cognitive decline in multiple domains.
  • In cognitively healthy individuals, high baseline plasma Aβ42 and decreasing/stable Aβ42 were linked to accelerated cognitive decline, primarily in memory.
  • These findings suggest a link between plasma Aβ and cognitive changes even before the onset of dementia.

Conclusions:

  • Plasma Aβ levels are associated with various cognitive changes, clarifying the previously observed downward trend of plasma Aβ with AD onset.
  • The strong association with memory in healthy individuals suggests plasma Aβ may indicate early neurological changes preceding dementia.
  • Plasma Aβ may serve as a potential biomarker for early cognitive impairment and AD risk.