02059nas a2200361   4500000000100000008004100001260001300042653000900055653002200064653001000086653002200096653002600118653001000144653001500154653001600169653001100185653002500196653001200221653001200233653002100245653001800266653001700284100001300301700001300314700001200327700001100339700001200350245010900362300001000471490000800481520119400489022001401683       1994                            d  c1994 Oct10aAged10aAged, 80 and over10aAging10aAlzheimer Disease10aAmyloid beta-Peptides10aBrain10aCell Count10aHippocampus10aHumans10aImmunohistochemistry10aleprosy10aNeurons10aReference Values10aTemporal Lobe10aTau Proteins1 aChui D H1 aTabira T1 aIzumi S1 aKoya G1 aOgata J00aDecreased beta-amyloid and increased abnormal Tau deposition in the brain of aged patients with leprosy.  a771-50 v1453 a<p>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 III (classical) plaques were significantly fewer (P < 0.05) in leprosy subjects compared with controls. Interestingly, neurofibrillary tangles in the temporal cortex were much more frequent in leprosy patients than in controls (P < 0.05). However, hippocampal CA3 pyramidal neurons in leprosy patients were well preserved. These data indicate that 1) leprosy patients have a low risk of A beta deposition but a high risk of abnormal tau deposition, 2) abnormal tau deposition is unrelated to A beta deposition in leprosy, and 3) neuronal loss is unrelated to abnormal tau deposition. It is not clear at present whether the result is related to the disease process itself, antileprosy treatment, environmental factors, or the genetic background in leprosy patients.</p>  a0002-9440