Publication Detail

The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.

Cellular localization of messenger RNA encoding amyloid-beta-protein in normal tissue and in Alzheimer disease.

D E Schmechel; D Goldgaber; D S Burkhart; J R Gilbert; D C Gajdusek; A D Roses (Profiled Authors: Roses, Allen D; Schmechel, Donald E; Gilbert, John R)

Department of Medicine, Duke University Medical Center, Durham, NC 27710.
Alzheimer disease and associated disorders 1988;2(2):96-111.

Amyloid precursor protein (APP) gene encodes the short peptide fragment amyloid-beta-protein present in senile plaque cores, cerebrovascular amyloid, and intracellular neurofibrillary tangles in Alzheimer disease (AD). Using in situ hybridization with biotin-labeled RNA probes, we found distinctive patterns of APP gene expression in different regions of postmortem human brain. Strong hybridization signal for APP messenger RNA (mRNA) was detected in specific classes of neurons, fascicular oligodendroglia, satellite glia, and presumptive microglia. Weaker signal was seen in other neuronal classes, fascicular astrocytes, and vascular endothelial cells, but no signal was seen in protoplasmic astrocytes. Human thymus also shows a restricted pattern of hybridization with high signal in reticular epithelial cells, and much lower signal in lymphocytes. In AD patients, neuronal hybridization for APP mRNA was specifically increased in hippocampus, but not cerebellar and visual cortex when compared to hybridization for neuron-specific enolase mRNA. Most neurons with neurofibrillary tangles had strong APP mRNA signal. These results suggest that APP gene expression is highly regulated in normal tissue, that many different cell classes in brain express the APP gene, and that neuronal expression may increase specifically in brain regions where widespread injury occurs in AD. Amyloid deposits in brains of AD patients might be explained by local production of precursor protein in endothelial cells, neurons or glia.

2 Originating Grant

• 1.

  Schmechel, Donald E

  ALZHEIMER'S DISEASE RESEARCH CENTER

  1 May 2000 - 30 April 2005

  NATIONAL INSTITUTE ON AGING

  Total Funding: $ 16,537,307

• 2.

  ROSES, ALLEN D

  ALZHEIMERS DISEASE RESEARCH CENTER

  30 September 1985 - 30 April 2000

  NATIONAL INSTITUTE ON AGING

  Total Funding: $ 17,660,528

Scientific Context

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