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Related Concept Videos

Amyloid Fibrils03:03

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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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Some solids can transition directly into the gaseous state, bypassing the liquid state, via a process known as sublimation. At room temperature and standard pressure, a piece of dry ice (solid CO2) sublimes, appearing to gradually disappear without ever forming any liquid. Snow and ice sublimate at temperatures below the melting point of water, a slow process that may be accelerated by winds and the reduced atmospheric pressures at high altitudes. When solid iodine is warmed, the solid sublimes...
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Aging01:26

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Characterization of Amyloid Structures in Aging C. Elegans Using Fluorescence Lifetime Imaging
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Subthreshold Amyloid Predicts Tau Deposition in Aging.

Stephanie L Leal1, Samuel N Lockhart2,3, Anne Maass2,4

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The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
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Early Alzheimer's detection is key. Even in those testing negative for amyloid-beta, its accumulation rate and levels predict tau buildup and memory decline, highlighting the need for early intervention.

Keywords:
PETagingamyloidmemorypreclinicaltau

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Area of Science:

  • Neuroscience
  • Gerontology
  • Biomarker Research

Background:

  • Current Alzheimer's disease (AD) detection relies on positive/negative amyloid-beta (Aβ) biomarker classification.
  • Aβ accumulation begins years before biomarker abnormality, necessitating earlier detection methods.
  • Understanding preclinical AD pathology is crucial for timely intervention.

Purpose of the Study:

  • To investigate the earliest changes in AD pathology and their impact on memory in cognitively normal older adults.
  • To explore the relationship between Aβ accumulation, tau deposition, and cognitive function.
  • To identify potential targets for early intervention in preclinical AD.

Main Methods:

  • Longitudinal [11C]Pittsburgh Compound B PET scanning and neuropsychological assessments in 71 cognitively normal older adults.
  • [18F]AV-1451 PET scanning to measure tau deposition in a subset (N=37).
  • Analysis of baseline Aβ levels, Aβ accumulation rates, and their correlation with tau pathology and memory decline.

Main Results:

  • An inverted-U relationship was observed between baseline Aβ levels and Aβ slope, indicating slowing Aβ accumulation even in normal adults.
  • In amyloid-negative participants, Aβ accumulation rate and baseline levels predicted early cortical tau deposition.
  • Amyloid measures only correlated with memory decline when baseline Aβ levels were elevated, suggesting pathology precedes cognitive impact.

Conclusions:

  • Amyloid measures are sensitive predictors of early tau deposition in preclinical AD.
  • Aβ accumulation may slow in preclinical AD, suggesting it's a later stage of progression.
  • Early intervention with amyloid-lowering therapies is crucial, even in individuals testing amyloid-negative, before significant cognitive decline.