Head trauma is considered to be a risk factor for Alzheimer's disease,
because a high prevalence of beta AP deposits has repeatedly been rep
orted in patients who died within a few days following head injury. To
evaluate this statement, we undertook two studies using immunohistoch
emistry 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 concentra
tion of antibody (dilution 1:2) we found beta AP diffuse deposits in o
ne 46-year-old case. In a second study, 17 patients aged 60-79 years o
ld, who died 1-35 days after head injury, were compared to a control g
roup. We did not find any significant difference in the density of bet
a AP diffuse deposits between cases and controls using usual dilutions
of beta AP antibody. The density of beta AP diffuse deposits was link
ed only to aging and the presence of senile plaques.