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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 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...
Aging01:26

Aging

Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
Cellular Clock Theory
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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...

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Related Experiment Video

Updated: Jun 15, 2026

Symmetric Bihemispheric Postmortem Brain Cutting to Study Healthy and Pathological Brain Conditions in Humans
08:29

Symmetric Bihemispheric Postmortem Brain Cutting to Study Healthy and Pathological Brain Conditions in Humans

Published on: December 18, 2016

Neurodegenerative changes in human aging brain. An autopsy study.

D Arsene1, Carmen Ardeleanu

  • 1Histopathology Department, Victor Babes National Institute for Research and Development in Pathology and Biomedical Sciences, Bucharest, Romania. dorelarsene@yahoo.com

Romanian Journal of Morphology and Embryology = Revue Roumaine De Morphologie Et Embryologie
|March 2, 2010
PubMed
Summary

Brain aging involves neurodegenerative changes like senile plaques and neurofibrillary tangles. While these lesions increase with age, their direct link to aging requires further human studies.

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Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains
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Last Updated: Jun 15, 2026

Symmetric Bihemispheric Postmortem Brain Cutting to Study Healthy and Pathological Brain Conditions in Humans
08:29

Symmetric Bihemispheric Postmortem Brain Cutting to Study Healthy and Pathological Brain Conditions in Humans

Published on: December 18, 2016

Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains
12:28

Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains

Published on: June 3, 2020

Area of Science:

  • Neurology
  • Neuroscience
  • Pathology

Background:

  • Neurodegenerative changes in the human brain often parallel the aging process.
  • Senile plaques and neurofibrillary tangles are key pathological hallmarks.
  • Understanding their relationship with aging is crucial for neurodegenerative disease research.

Purpose of the Study:

  • To prospectively characterize cortical senile plaques and neurofibrillary tangles in adult human subjects.
  • To determine if aging is associated with increased burden of these lesions.
  • To investigate the cortical distribution of lesions irrespective of mental status.

Main Methods:

  • Post-mortem examination of 55 adult human subjects across a wide age spectrum (30-97 years).
  • Immunohistochemistry for amyloid-beta (Abeta) and tau protein.
  • ApoE genotyping in 33 cases via polymerase chain reaction.

Main Results:

  • Brain Abeta deposition (senile plaques) was observed only in subjects over 65 years old.
  • Abeta accumulation strongly correlated with the presence of neurofibrillary tangles.
  • Notably, some very elderly individuals lacked both Abeta and tau-positive lesions.

Conclusions:

  • Abeta and tau protein deposition show a predilection for the aging brain.
  • The direct relationship between these pathological hallmarks and the aging process warrants further investigation in human subjects.
  • Individual variability exists in the manifestation of these age-related brain changes.