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Related Concept Videos

Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

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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...
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Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

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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...
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Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

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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...
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Aging01:26

Aging

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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
The cellular clock theory posits that the human lifespan is closely tied to the finite capacity of cells to divide, a phenomenon governed by telomeres, which are protective caps at the ends of...
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Dementia l: Introduction01:22

Dementia l: Introduction

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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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Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

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Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...
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Neuropathological changes in aging brain.

Aikaterini Xekardaki1, Eniko Kövari, Gabriel Gold

  • 1Department of Mental Health and Psychiatry, University Hospitals of Geneva, Geneva, Switzerland, Aikaterini.Xekardaki@hcuge.ch.

Advances in Experimental Medicine and Biology
|November 23, 2014
PubMed
Summary
This summary is machine-generated.

Alzheimer's disease (AD) neurofibrillary tangles (NFTs) in specific brain regions correlate more strongly with cognitive decline than beta-amyloid plaques. Understanding this relationship is crucial for developing better AD diagnostics and treatments.

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Area of Science:

  • Neuropathology
  • Neuroscience
  • Gerontology

Background:

  • Alzheimer's disease (AD) is characterized by neurofibrillary tangles (NFTs) and beta-amyloid (Aβ) plaques.
  • The precise correlation between these neuropathological hallmarks and cognitive decline remains incompletely understood.
  • Both NFTs and Aβ plaques are observed in normal aging, complicating their specific association with AD.

Purpose of the Study:

  • To review studies assessing the correlation between neuropathological lesions and clinical expression of Alzheimer's disease.
  • To investigate the differential impact of NFTs and Aβ plaques on cognitive status.
  • To explore the concept of cognitive reserve in mitigating the effects of AD pathology.

Main Methods:

  • Review of neuropathological studies conducted over two decades.
  • Correlation analysis of NFT counts in CA1 and entorhinal cortex with cognitive status.
  • Analysis of beta-amyloid load in relation to cognitive decline.
  • Consideration of the cognitive reserve theory.

Main Results:

  • The number of NFTs in the CA1 and entorhinal cortex appears more closely linked to cognitive status than amyloid plaque load.
  • The role of amyloid load in Alzheimer's disease progression is still considered controversial.
  • The theory of cognitive reserve offers a framework for understanding individual differences in compensation for neuropathology.

Conclusions:

  • Neurofibrillary tangle burden, particularly in specific brain regions, may be a more significant correlate of cognitive decline in Alzheimer's disease than amyloid plaques.
  • Further research into cognitive reserve is essential for understanding resilience to AD pathology.
  • There is an urgent need for improved therapeutic and early diagnostic strategies for Alzheimer's disease due to its increasing prevalence and societal cost.