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Journal Article

Citation

Adle-Biassette H, Duyckaerts C, Wasowicz M, He Y, Fornes P, Foncin JF, Lecomte D, Hauw JJ. Neurobiol. Aging 1996; 17(3): 415-419.

Affiliation

Laboratoire de Neuropathologie R. Escourolle, Hôpital de la Salpêtrière, Paris, France.

Copyright

(Copyright © 1996, Elsevier Publishing)

DOI

unavailable

PMID

8725903

Abstract

Head trauma is considered to be a risk factor for Alzheimer's disease, because a high prevalence of beta AP deposits has repeatedly been reported in patients who died within a few days following head injury. To evaluate this statement, we undertook two studies using immunohistochemistry for beta AP and found a surprisingly low prevalence of beta AP diffuse deposits. We first selected 23 patients aged 17-63 years, who died 0-76 days after head trauma. Using beta AP antibody at the usual dilution (1:100), we did not find any deposits. With a high concentration of antibody (dilution 1:2) we found beta AP diffuse deposits in one 46-year-old case. In a second study, 17 patients aged 60-79 years old, who died 1-35 days after head injury, were compared to a control group. We did not find any significant difference in the density of beta AP diffuse deposits between cases and controls using usual dilutions of beta AP antibody. The density of beta AP diffuse deposits was linked only to aging and the presence of senile plaques.


Language: en

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