title: Tau, paired helical filaments and amyloid in the neocortex: a morphometric study of 15 cases with graded intellectual status in aging and senile dementia of Alzheimer type.
abstract: Tau immunoreactivity was studied in temporal neocortex, area 22, in 15 cases with graded intellectual status and compared with the immunoreactivity observed with an antiserum against paired helical filaments (PHF) and with the density of amyloid revealed by thioflavin S. Samples came from women over 75 years either intellectually normal or affected by senile dementia of the Alzheimer type at various degrees of severity. Mental status had been prospectively assessed by the Blessed's test score. Anti-tau labelled a neuropil meshwork, the density of which increased with the severity of the disease. This meshwork was denser in layers II, III and V in the most affected cases. The number and the size of the tau-positive fibers within the senile plaques increased with the intellectual deficit. Senile plaques were more numerous in layers II and III and neurofibrillary tangles in layers III and V whatever the staining technique: tau or PHF immunocytochemistry, and thioflavin S. The densities of senile plaques and of neurofibrillary tangles (NFT) were correlated with the severity of the disease whatever the staining method. The three methods revealed a systematically different number of changes. This systematic difference could greatly influence the neuropathological diagnosis. It could be the consequence of various factors: different sensitivities of the staining methods or changes in the antigenic and amyloid composition of the lesion according to the stage of the disease. In line with the last hypothesis, a higher proportion of amyloid-rich plaques was noted in the less affected cases, suggesting that tau and PHF epitopes appeared secondarily.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Laboratoire R. Escourolle, Hôpital de la Salpêtrière, Paris, France.
authors.forename: P
authors.initials: P
authors.lastname: Delaère
authors.forename: C
authors.initials: C
authors.lastname: Duyckaerts
authors.forename: J P
authors.initials: JP
authors.lastname: Brion
authors.forename: V
authors.initials: V
authors.lastname: Poulain
authors.forename: J J
authors.initials: JJ
authors.lastname: Hauw
mesh_terms: D000368:Aged; D000375:Aging / Q000473:pathology*; D000544:Alzheimer Disease / Q000150:complications / Q000473:pathology*; D000682:Amyloid / Q000378:metabolism*; D002540:Cerebral Cortex / Q000254:growth & development / Q000473:pathology*; D003072:Cognition Disorders / Q000473:pathology*; D003599:Cytoskeleton / Q000473:pathology*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007382:Intermediate Filaments / Q000378:metabolism / Q000473:pathology*; D008869:Microtubule-Associated Proteins / Q000378:metabolism*; D016875:tau Proteins
chemical_list: D000682:Amyloid; D008869:Microtubule-Associated Proteins; D016875:tau Proteins