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Alzheimer Disease.

Estela Area-Gomez1, Eric A Schon2,3

  • 1Department of Neurology, Columbia University Medical Center, 630 West 168th Street, New York, NY, 10032, USA.

Advances in Experimental Medicine and Biology
|August 18, 2017
PubMed
Summary
This summary is machine-generated.

Mitochondria-associated ER membranes (MAM) dysfunction, not just amyloid plaques, may drive Alzheimer disease (AD) progression. Early alterations in MAM function are linked to AD pathogenesis.

Keywords:
ApoECholesterolCholesteryl estersEndoplasmic reticulumLipid raftsMAMMembranesMitochondriaMitochondria-associated ER membranesNeurodegenerationPhospholipids

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Alzheimer disease (AD) pathogenesis is often explained by the amyloid cascade hypothesis.
  • However, early AD features include altered metabolism and mitochondrial dysfunction preceding plaque and tangle formation.

Purpose of the Study:

  • To investigate the role of mitochondria-associated ER membranes (MAM) in Alzheimer disease pathogenesis.
  • To explore the connection between MAM function and early AD biochemical and morphological changes.

Main Methods:

  • Analysis of cellular and animal models of AD.
  • Examination of cells from AD patients.
  • Biochemical and morphological assessments of MAM and mitochondria.

Main Results:

  • Mitochondria-associated ER membranes (MAM) are closely apposed to mitochondria and involved in lipid metabolism.
  • MAM-localized functions are significantly increased in various AD models and patient cells.
  • These MAM alterations appear early in the disease course, before significant plaque and tangle accumulation.

Conclusions:

  • Increased ER-mitochondria connectivity and MAM function are fundamental to Alzheimer disease pathogenesis.
  • MAM dysfunction offers a potential explanation for early biochemical and morphological alterations in AD.
  • Targeting MAM may represent a novel therapeutic strategy for Alzheimer disease.