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Related Concept Videos

Amyloid Fibrils03:03

Amyloid Fibrils

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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Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
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Magnesium modulates amyloid-beta protein precursor trafficking and processing.

Jia Yu1, Miao Sun, Zheng Chen

  • 1Neuroscience Research Institute & Department of Neurobiology, Key Laboratory for Neuroscience, Ministry of Education & Ministry of Public Health, Health Science Center, Peking University, Beijing, China Beijing Geriatric Hospital, Beijing, China.

Journal of Alzheimer'S Disease : JAD
|April 24, 2010
PubMed
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Magnesium levels impact Alzheimer

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Area of Science:

  • Neuroscience
  • Biochemistry

Background:

  • Alzheimer's disease (AD) involves amyloid-beta (Abeta) plaque accumulation.
  • Magnesium is crucial for neuronal function, and its levels are reduced in AD patients.
  • The precise role of magnesium in AD pathogenesis is not fully understood.

Purpose of the Study:

  • To investigate how extracellular magnesium concentrations affect amyloid-beta protein precursor (AbetaPP) processing and Abeta secretion.
  • To determine the impact of varying magnesium levels on the pathways of AbetaPP cleavage.

Main Methods:

  • Cells were treated with physiological, low, and high extracellular magnesium concentrations ([Mg2+]o).
  • AbetaPP processing, Abeta secretion, and cell viability were assessed over time.
  • Levels of AbetaPP, its C-terminal fragments (CTFs), and soluble sAbetaPPalpha were quantified.

Main Results:

  • High [Mg2+]o increased alpha-secretase activity, leading to higher CTFalpha and sAbetaPPalpha release.
  • Low [Mg2+]o promoted beta-secretase activity, increasing CTFbeta accumulation and Abeta secretion.
  • Magnesium deprivation impaired cell viability, which was reversible upon restoring physiological magnesium levels.

Conclusions:

  • Extracellular magnesium concentration modulates AbetaPP processing in a time- and dose-dependent manner.
  • High magnesium levels favor the non-amyloidogenic alpha-secretase pathway.
  • Magnesium supplementation may hold therapeutic potential for preventing Alzheimer's disease.