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Alzheimer Disease ll: Pathophysiology01:23

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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 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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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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Apolipoprotein E pathology in vascular dementia.

Troy T Rohn1, Ryan J Day1, Colin B Sheffield1

  • 1Department of Biological Sciences, Boise State University Boise, ID 83725, USA.

International Journal of Clinical and Experimental Pathology
|April 4, 2014
PubMed
Summary

Researchers found a fragment of apolipoprotein E (apoE) within neurofibrillary tangles in vascular dementia (VaD) brains. This suggests apoE cleavage plays a role in VaD, supporting APOE gene polymorphism as a risk factor.

Keywords:
PHF-1Vascular dementiaapoEapolipoprotein Eastrocytesimmunohistochemistryneurofibrillary tanglesplaques

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Area of Science:

  • Neuroscience
  • Pathology
  • Genetics

Background:

  • Vascular dementia (VaD) is the second leading cause of dementia, characterized by cerebrovascular disease and ischemic events.
  • Apolipoprotein E (apoE) gene polymorphism is a suspected risk factor for VaD, yet post-mortem studies on apoE brain pathology are limited.

Purpose of the Study:

  • To investigate the potential role of apolipoprotein E (apoE) protein in the pathology of vascular dementia (VaD).
  • To examine apoE presence in the brains of VaD patients using immunohistochemistry.

Main Methods:

  • Analysis of seven confirmed VaD cases using immunohistochemistry.
  • Utilized a specific antibody (nApoECF) targeting the amino-terminal fragment of apoE.
  • Examined APOE genotypes (3/3, 3/4, 4/4) and co-localization with PHF-1 in neurofibrillary tangles (NFTs).

Main Results:

  • The nApoECF antibody consistently labeled neurofibrillary tangles (NFTs), blood vessels, and reactive astrocytes in VaD brains.
  • nApoECF staining co-localized with PHF-1 in NFTs, primarily in layer II neurons of the entorhinal cortex.
  • Approximately 38.4% of identified NFTs contained the amino-terminal fragment of apoE across different APOE genotypes.

Conclusions:

  • These findings support a role for the proteolytic cleavage of apoE in the pathogenesis of VaD.
  • The results reinforce previous evidence linking APOE polymorphism to increased susceptibility to vascular dementia.