Localization of β-secretase memapsin 2 in the brain of Alzheimer's patients and normal aged controls

Anyang Sun, Gerald Koelsch, Jordan Tang, Guoying Bing

Research output: Contribution to journalArticlepeer-review

40 Scopus citations


Chronic accumulation of β-amyloid in the brain has been shown to result in complex molecular and cellular changes that accompany neurodegeneration in Alzheimer's disease (AD). In this study, we examined the expression of a newly identified β-secretase, memapsin 2 (M2) or β-site APP cleaving enzyme in deparaffinized sections from 10 AD patients and 10 aged matched controls and in frozen samples of parietal cortex from 11 AD and 8 controls. M2 is mainly expressed in neurons, with high levels in CA4 to CA2 regions and transentorhinal cortex and low or intermediate levels in CA1, subiculum, and granule cells of the dentate gyrus. The majority of AD brains showed an increase of M2 expression in the CA1, but a decrease in the transentorhinal cortex. A subset of controls and AD patients had high M2 expression in parietal neocortex. Double-staining revealed that senile plaques are not directly associated with the soma of M2-expressing neurons. Neurofibrillary tangles were associated with lower M2 expression in AD. These data indicate that β-secretase M2 may not be straightforwardly involved in amyloid plaque formation in AD brain.

Original languageEnglish
Pages (from-to)10-22
Number of pages13
JournalExperimental Neurology
Issue number1
StatePublished - 2002

Bibliographical note

Funding Information:
Human brain sections used in this study were kindly provided by the University of Kentucky Alzheimer’s Disease Research Center headed by Dr. William R. Markesbery. This work was supported by NIH Grant 3R01 NS39345-01 (G.B.).


  • Alzheimer's disease
  • Memapsin 2
  • Neurofibrillary tangles
  • Senile plaques
  • β-amyloid
  • β-secretase

ASJC Scopus subject areas

  • Neurology
  • Developmental Neuroscience


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