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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...
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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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Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains
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Primary progressive aphasia: clinicopathological correlations.

Murray Grossman1

  • 1Department of Neurology, 2 Gibson, Hospital of the University of Pennsylvania, Philadelphia, PA 19104-4283, USA. mgrossma@mail.med.upenn.edu

Nature Reviews. Neurology
|February 9, 2010
PubMed
Summary
This summary is machine-generated.

Primary progressive aphasia (PPA) involves language decline from neurodegenerative diseases. Identifying the specific pathology behind PPA variants is crucial for targeted treatments and clinical trials.

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Area of Science:

  • Neurology
  • Neuroscience
  • Pathology

Background:

  • Primary progressive aphasia (PPA) is a language disorder often presenting as a neurodegenerative disease, commonly frontotemporal lobar degeneration.
  • Recognized PPA variants include progressive nonfluent aphasia, semantic dementia, and logopenic progressive aphasia.

Purpose of the Study:

  • To highlight the critical need for determining the histopathological basis of PPA for developing etiology-specific treatments.
  • To review clinicopathological correlations in PPA, emphasizing the roles of tauopathies, TDP-43 proteinopathies, and Alzheimer disease.

Main Methods:

  • Review of clinicopathological data in PPA cases.
  • Discussion of emerging neuroimaging and biofluid biomarkers for diagnosis.

Main Results:

  • Clinicopathological correlations reveal contributions from tauopathies, TDP-43 proteinopathies, and Alzheimer disease to PPA.
  • While associations exist between PPA variants and specific pathologies, many cases present with unexpected underlying pathologies.

Conclusions:

  • Accurate pathological diagnosis of PPA is essential for advancing treatment strategies.
  • Integrating biomarker assessments with clinical examination offers hope for precise in-vivo pathological diagnosis of PPA.
  • Such diagnostic advancements are vital for facilitating targeted clinical trials for PPA spectrum diseases.