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N Behrouz

Publications and source records attributed to N Behrouz.

7 recordsLinked to original sources
PubMed1991

The immunohistochemical evidence of amyloid diffuse deposits as a pathological hallmark in Alzheimer's disease.

We performed an immunocytochemical study of cerebral cortex from cases of Alzheimer's disease and from aged nondemented controls, using periodic acid pretreatment and polyclonal beta-protein antibodies. In addition to senile plaques (SP) and amyloid angiopathy (AA), the beta-protein antibodies detected band-like deposits present throughout the cortical layers. Moreover, large plaque-like infiltrations with diffuse and amorphous characteristics were observed in the cortical gray and white matter, and these deposits were often associated with capillaries. Our results suggest that an abundance of these lesions, which were detected only with this immunostaining procedure in Alzheimer cortex, may be characteristic of Alzheimer's disease.

Aged↗
PubMed1990

[Alzheimer's disease: the beta amyloid protein A4 is also present in the cortical white matter].

Amyloid deposits constituted with the beta amyloid protein A4 (beta PA4) have been recently immunodetected in skin and intestine wall of Alzheimer's patients. These findings support the hypothesis of an extraneuronal origin of the beta PA4. Until now, these amyloid deposits had not been observed in the white matter of Alzheimer's brains. Using an antiserum against the 1-10 N Ter subsequence of the beta PA4, we immunodetected amyloid deposits in white matter sections of Alzheimer's brains, pretreated with periodic acid. The immunolabelled amyloid substance was associated with capillaries. These original findings are in good agreement with the vascular origin of the beta PA4.

Aged↗
PubMed1989

An antiserum to the N-terminal subsequence of the Alzheimer amyloid beta protein does not react with neurofibrillary tangles.

Polyclonal antibodies were raised against a synthetic peptide corresponding to a subsequence for the first 10 residues of the beta amyloid protein A4 (1-10 beta PA4). In an immunoperoxidase study of Alzheimer brain tissue, these antibodies immunostained senile plaque cores, amyloid vessel walls, and amyloid fibrils surrounding senile plaques and angiopathic vessels. Neurofibrillary tangles stained with thioflavin S or immunostained with anti-Tau immune serum were never immunodetected with the anti 1-10 beta PA4. We confirm that the neurofibrillary tangles do not contain epitopes corresponding to the first 10 residues of the beta PA4.

Alzheimer Disease↗
PubMed1989

Alzheimer's disease: glycolytic pretreatment dramatically enhances immunolabeling of senile plaques and cerebrovascular amyloid substance.

In Alzheimer's disease, three types of pathologic lesions are stained by thioflavin: neurofibrillary tangles, senile plaques, and amyloidaceous vessels. We have used anti-beta protein amyloid A4 and anti-tau protein antisera and compared immunolabeling with thioflavin staining. Anti-tau detected only neurofibrillary tangles; anti-beta-PA4 immunostained senile plaques and amyloidaceous vessels. Glycolytic pretreatment (2% periodic acid overnight or glycosidases digestion) dramatically enhanced the anti-beta-PA4 immunolabeling of senile plaques, amyloidaceous vessels, and a previously undetected extracellular substance; neurofibrillary tangles were never immunostained. Therefore, glycolytic pretreatment exposes buried epitopes in the amyloid and is a good method for amplification of immunostaining. The nature of the interaction between saccharides and beta-protein amyloid A4 is unknown.

Alzheimer Disease↗
PubMed1989

[Alzheimer's disease: immunohistochemical characterization of cerebral amyloid deposits].

In Alzheimer cortex tissue sections, thioflavine stained three patterns of amyloid lesions: neurofibrillary tangles (NFT), senile plaques (SP) and vessel walls (amyloid angiopathy AA). An anti serum against Tau proteins detected NFT but neither SP nor AA. In contrast, an anti serum against beta protein amyloid (BP A4) revealed SP and AA but not NFT. A periodic acid pretreatment dramatically enhanced the anti-BP A4 immunolabelling corresponding to microplaques as well as a large amount of diffuse extracellular amyloid substance, but never stained NFT. Pretreatment of tissue sections with a mixture of endo and exoglycosidases gave identical results and corroborates the extraneuronal processing of BP A4 that appears in a glycosylated form in the extracellular compartment.

Alzheimer Disease↗