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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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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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Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
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Amyloid Fibrils03:03

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Related Experiment Video

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Visualization of Amyloid &#946; Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry
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Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry

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Beta-amyloid deposition and the aging brain.

Karen M Rodrigue1, Kristen M Kennedy, Denise C Park

  • 1Center for BrainHealth, School of Behavioral and Brain Sciences, The University of Texas at Dallas, 2200 W. Mockingbird Ln, Dallas, TX 75235, USA.

Neuropsychology Review
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PubMed
Summary

Beta amyloid (Abeta) deposition is an early marker for cognitive aging. This review explores how Abeta imaging in Alzheimer's Disease, mild cognitive impairment, and healthy adults reveals its impact on cognitive decline.

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Area of Science:

  • Cognitive Neuroscience
  • Neuroimaging
  • Aging Research

Background:

  • Identifying neural mechanisms for cognitive aging is crucial.
  • Beta amyloid (Abeta) deposition is a promising biomarker for cognitive aging.
  • Abeta imaging reveals deposition in Alzheimer's Disease (AD), Mild Cognitive Impairment (MCI), and healthy adults.

Purpose of the Study:

  • To review studies on Abeta deposition imaging.
  • To examine the cognitive consequences of Abeta deposition.
  • To explore the role of genetic risk and cognitive reserve in cognitive aging.

Main Methods:

  • Review of studies utilizing Abeta deposition imaging.
  • Analysis of radiotracer development for Abeta detection.
  • Synthesis of data from AD, MCI, and healthy adult populations.

Main Results:

  • Significant Abeta deposition is found in a substantial portion of healthy older adults.
  • Abeta deposition often precedes cognitive decline.
  • Abeta may initiate a cascade leading to age-related cognitive decline.

Conclusions:

  • Abeta imaging is vital for understanding cognitive aging.
  • Early detection of Abeta deposition can inform interventions.
  • Genetic risk and cognitive reserve modulate the effects of Abeta on cognition.