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BACE2 expression increases in human neurodegenerative disease.

Christopher J Holler1, Robin L Webb, Ashley L Laux

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The American Journal of Pathology
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Beta-secretase 2 (BACE2) levels and activity increase early in Alzheimer's disease (AD) and frontotemporal dementia, suggesting a shared role with BACE1 in neurological disorders.

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Pathology

Background:

  • Beta-secretase (BACE) enzymes are crucial for amyloid-beta (Aβ) peptide production, a key factor in Alzheimer's disease (AD) therapeutics.
  • While BACE1 is known to increase in late-stage AD, the role of BACE2 remains less understood.

Purpose of the Study:

  • To investigate the role and expression patterns of BACE2 in preclinical to late-stage Alzheimer's disease.
  • To compare BACE2 expression in AD with other neurological conditions like frontotemporal dementia and Down's syndrome.

Main Methods:

  • Detailed examination of BACE2 protein and enzymatic activity in human brain samples across different disease stages and controls.
  • Analysis of BACE2 mRNA levels, including splice variants, and correlation with protein and activity.
  • Comparative analysis of BACE1 and BACE2 expression across various neurological conditions.

Main Results:

  • BACE2 protein and enzymatic activity were elevated as early as preclinical AD and found in neurons and astrocytes.
  • Increased expression of BACE2 splice form C (lacking exon 7) paralleled BACE2 protein and activity.
  • BACE1 and BACE2 levels were strongly correlated, suggesting shared regulatory mechanisms.
  • BACE2 was elevated in frontotemporal dementia but not in Down's syndrome, irrespective of Aβ deposition.

Conclusions:

  • Both BACE1 and BACE2 expression are linked and may jointly contribute to human neurological diseases.
  • Understanding the functions of BACE1 and BACE2 in different disease states is vital for developing effective AD therapeutics.