While neuropathological studies have established the pathology of dementia
pugilistica to be similar to that of Alzheimer's disease, there is little i
nformation about the early histological changes caused by the repetitive tr
auma that eventually produces dementia pugilistica. We have examined the br
ains of four young men and a frontal lobectomy specimen from a fifth, age r
ange 23-28 years, all of whom suffered mild chronic head injury. There were
two boxers, a footballer, a mentally subnormal man with a long history of
head banging, and an epileptic patient who repeatedly hit his head during s
eizures. The four autopsy cases were widely sampled; the lobectomy specimen
was serially sliced after fixation. Routine stains were performed; immunos
taining included P-amyloid precursor protein, amyloid beta-protein (A beta)
, tau and apolipoprotein E (apoE). Pathological findings in all five cases
were of neocortical neurofibrillary tangles (NFTs) and neuropil threads, wi
th groups of tangles consistently situated around blood vessels in the wors
t affected regions. No A beta immunoreactivity was detected. The amount of
neuronal apoE expression varied widely between the cases with no clear rela
tion to the NFTs. The apoE genotype was determined in only two cases (both
epsilon 3/epsilon 3). It appears that repetitive head injury in young adult
s is initially associated with neocortical NFT formation in the absence of
A beta deposition. The distribution of the tau pathology suggests that the
pathogenesis of cytoskeletal abnormalities may involve damage to blood vess
els or perivascular elements.