We probed serial and near serial sections of cerebellum from 13 Alzhei
mer's disease (AD), 10 older Down's syndrome (DS) patients, and 9 age-
matched, non-AD controls, using single and double labeling immunohisto
chemistry to investigate the pathologic consequences of beta-amyloid o
r A4 (A beta) deposits in cerebellum and their relationship to Purkinj
e cells (PCs). Our data showed that A beta deposits in cerebellum of A
D and older DS adults only form diffuse or preamyloid plaques and the
density of A beta lesions per unit area of molecular layer correlated
with the number of PCs per unit length of the subjacent PC layer in do
uble immunostained sections (r = 0.85; p<0.001). About 65% of these ce
rebellar A beta deposits were in physical contact with PC dendrites. N
o A beta plaques were found in the cerebellum of controls. Despite the
abundance of A beta deposits in the cerebellar cortex of AD and older
DS patients, neither PC bodies nor PC dendrites in physical contact w
ith A beta lesions showed evidence of structural abnormalities.