Dh. Chui et al., DECREASED BETA-AMYLOID AND INCREASED ABNORMAL TAU-DEPOSITION IN THE BRAIN OF AGED PATIENTS WITH LEPROSY, The American journal of pathology, 145(4), 1994, pp. 771-775
We examined the brains of 37 leprosy patients (mean age, 76.3 +/- 7.8
years), 5 patients with Alzheimer-type dementia (mean age, 79.0 +/- 9.
5 years), and 23 age-matched non-dementia controls (mean age, 77.6 +/-
5.4 years). The frequency of beta-amyloid (A beta)-positive cases was
lower (27. 0%) in leprosy patients (n = 37) than in controls (47.8%;
P = 0.05, Z = 1.49). When senile plaque subtypes were examined, type I
II (classical) plaques were significantly fewer (P < 0.05) in leprosy
subjects compared with controls. Interestingly, neurofibrillary tangle
s in the temporal cortex were much more frequent in leprosy patients t
han in controls (P < 0.05). However hippocampal CA3 pyramidal neurons
in leprosy patients were well preserved. These data indicate that 1) l
eprosy patients have a low risk of A beta deposition but a high risk o
f abnormal tau deposition, 2) abnormal tau deposition is unrelated to
AP deposition in leprosy, and 3) neuronal loss is unrelated to abnorma
l tau deposition It is not clear at present whether the result is rela
ted to the disease process itself, antileprosy treatment, environmenta
l factors, or the genetic background in leprosy patients.