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Neuronal and nonneuronal quantitative BACE immunocytochemical expression in the entorhinohippocampal and frontal regions in Alzheimer's disease.
Dement Geriatr Cogn Disord. 2005; 19(4):171-83.DG

Abstract

In this study, we quantitatively investigated the expression of beta-site amyloid precursor protein cleaving enzyme (BACE) in the entorhinohippocampal and frontal cortex of Alzheimer's disease (AD) and old control subjects. The semiquantitative estimation indicated that the intensity of BACE overall immunoreactivity did not differ significantly between AD and controls, but that a significantly stronger staining was observed in the hippocampal regions CA3-4 compared to other regions in both AD patients and controls. The quantitative estimation confirmed that the number of BACE-positive neuronal profiles was not significantly decreased in AD. However, some degeneration of BACE-positive profiles was attested by the colocalization of neurons expressing BACE and exhibiting neurofibrillary tangles (NFT), as well as by a decrease in the surface area of BACE-positive profiles. In addition, BACE immunocytochemical expression was observed in and around senile plaques (SP), as well as in reactive astrocytes. BACE-immunoreactive astrocytes were localized in the vicinity or close to the plaques and their number was significantly increased in AD entorhinal cortex. The higher amount of beta-amyloid SP and NFT in AD was not correlated with an increase in BACE immunoreactivity. Taken together, these data accent that AD progression does not require an increased neuronal BACE protein level, but suggest an active role of BACE in immunoreactive astrocytes. Moreover, the strong expression in controls and regions less vulnerable to AD puts forward the probable existence of alternate BACE functions.

Authors+Show Affiliations

Center for Psychiatric Neuroscience and Service of Old Age Psychiatry, Department of Psychiatry-CHUV, University of Lausanne, CH-1008 Lausanne, Switzerland. Genevieve.Leuba@hospvd.chNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

15677864

Citation

Leuba, Geneviève, et al. "Neuronal and Nonneuronal Quantitative BACE Immunocytochemical Expression in the Entorhinohippocampal and Frontal Regions in Alzheimer's Disease." Dementia and Geriatric Cognitive Disorders, vol. 19, no. 4, 2005, pp. 171-83.
Leuba G, Wernli G, Vernay A, et al. Neuronal and nonneuronal quantitative BACE immunocytochemical expression in the entorhinohippocampal and frontal regions in Alzheimer's disease. Dement Geriatr Cogn Disord. 2005;19(4):171-83.
Leuba, G., Wernli, G., Vernay, A., Kraftsik, R., Mohajeri, M. H., & Saini, K. D. (2005). Neuronal and nonneuronal quantitative BACE immunocytochemical expression in the entorhinohippocampal and frontal regions in Alzheimer's disease. Dementia and Geriatric Cognitive Disorders, 19(4), 171-83.
Leuba G, et al. Neuronal and Nonneuronal Quantitative BACE Immunocytochemical Expression in the Entorhinohippocampal and Frontal Regions in Alzheimer's Disease. Dement Geriatr Cogn Disord. 2005;19(4):171-83. PubMed PMID: 15677864.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuronal and nonneuronal quantitative BACE immunocytochemical expression in the entorhinohippocampal and frontal regions in Alzheimer's disease. AU - Leuba,Geneviève, AU - Wernli,Gwenaëlle, AU - Vernay,André, AU - Kraftsik,Rudolf, AU - Mohajeri,M Hasan, AU - Saini,Krishan D, Y1 - 2005/01/25/ PY - 2004/07/16/accepted PY - 2005/1/29/pubmed PY - 2005/7/16/medline PY - 2005/1/29/entrez SP - 171 EP - 83 JF - Dementia and geriatric cognitive disorders JO - Dement Geriatr Cogn Disord VL - 19 IS - 4 N2 - In this study, we quantitatively investigated the expression of beta-site amyloid precursor protein cleaving enzyme (BACE) in the entorhinohippocampal and frontal cortex of Alzheimer's disease (AD) and old control subjects. The semiquantitative estimation indicated that the intensity of BACE overall immunoreactivity did not differ significantly between AD and controls, but that a significantly stronger staining was observed in the hippocampal regions CA3-4 compared to other regions in both AD patients and controls. The quantitative estimation confirmed that the number of BACE-positive neuronal profiles was not significantly decreased in AD. However, some degeneration of BACE-positive profiles was attested by the colocalization of neurons expressing BACE and exhibiting neurofibrillary tangles (NFT), as well as by a decrease in the surface area of BACE-positive profiles. In addition, BACE immunocytochemical expression was observed in and around senile plaques (SP), as well as in reactive astrocytes. BACE-immunoreactive astrocytes were localized in the vicinity or close to the plaques and their number was significantly increased in AD entorhinal cortex. The higher amount of beta-amyloid SP and NFT in AD was not correlated with an increase in BACE immunoreactivity. Taken together, these data accent that AD progression does not require an increased neuronal BACE protein level, but suggest an active role of BACE in immunoreactive astrocytes. Moreover, the strong expression in controls and regions less vulnerable to AD puts forward the probable existence of alternate BACE functions. SN - 1420-8008 UR - https://www.unboundmedicine.com/medline/citation/15677864/Neuronal_and_nonneuronal_quantitative_BACE_immunocytochemical_expression_in_the_entorhinohippocampal_and_frontal_regions_in_Alzheimer's_disease_ L2 - https://www.karger.com?DOI=10.1159/000083496 DB - PRIME DP - Unbound Medicine ER -