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Expression of differential immune factors in temporal cortex and cerebellum: the role of alpha-1-antichymotrypsin, apolipoprotein E, and reactive glia in the progression of Alzheimer's disease.
J Comp Neurol 1998; 396(4):511-20JC

Abstract

A variety of factors and processes have been implicated in the development and progression of the pathology of Alzheimer's Disease (AD), including amyloid fragment deposition, reactive gliosis, alpha-1-antichymotrypsin (ACT), and apolipoprotein E (APOE). Carriers of the APOE 4 allele have been shown to have an enhanced risk of developing AD, and the ACT signal peptide A/A genotype may modify the APOEepsilon4 risk. The protein products of these genes have been shown to enhance conversion of diffuse beta amyloid (Abeta) fibrils, which are found in diffuse plaques, to the fibrillar form found in neuritic plaques. In affected regions of AD brain, ACT and APOE colocalize with Abeta deposits and reactive microglia and astrocytes. We examined the regional distribution of ACT, APOE, and reactive glia in temporal cortex, where neuritic plaques are abundant, and cerebellum (in areas where diffuse plaques but not neuritic plaques accumulate) to examine the relationship of these markers to the deposition of Abeta. In temporal cortex, ACT and APOE staining was localized to plaque-like profiles, reactive astrocytes, and blood vessels; human leukocyte antigen-DR (HLA-DR) and glial fibrillary acidic protein (GFAP) staining revealed focal clusters of reactive microglia and astrocytes. In cerebellum, ACT and APOE immunoreactivity was never localized to plaque-like profiles but was weakly localized to unreactive astrocytes; weak HLA-DR and GFAP immunoreactivity was present on quiescent microglia throughout the cerebellum. The lack of fibrillar amyloid deposits in cerebellum, despite the presence of well-characterized markers thought to mediate the production of Abeta, suggests that this brain region may be lacking certain factors necessary for fibril formation or that the cerebellum responds differently to stimuli that successfully mediate inflammation in affected cortex.

Authors+Show Affiliations

Department of Psychiatry, Western Psychiatric Institute and Clinic and Graduate School of Public Health, University of Pittsburgh, Pennsylvania 15261, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

9651008

Citation

Styren, S D., et al. "Expression of Differential Immune Factors in Temporal Cortex and Cerebellum: the Role of Alpha-1-antichymotrypsin, Apolipoprotein E, and Reactive Glia in the Progression of Alzheimer's Disease." The Journal of Comparative Neurology, vol. 396, no. 4, 1998, pp. 511-20.
Styren SD, Kamboh MI, DeKosky ST. Expression of differential immune factors in temporal cortex and cerebellum: the role of alpha-1-antichymotrypsin, apolipoprotein E, and reactive glia in the progression of Alzheimer's disease. J Comp Neurol. 1998;396(4):511-20.
Styren, S. D., Kamboh, M. I., & DeKosky, S. T. (1998). Expression of differential immune factors in temporal cortex and cerebellum: the role of alpha-1-antichymotrypsin, apolipoprotein E, and reactive glia in the progression of Alzheimer's disease. The Journal of Comparative Neurology, 396(4), pp. 511-20.
Styren SD, Kamboh MI, DeKosky ST. Expression of Differential Immune Factors in Temporal Cortex and Cerebellum: the Role of Alpha-1-antichymotrypsin, Apolipoprotein E, and Reactive Glia in the Progression of Alzheimer's Disease. J Comp Neurol. 1998 Jul 13;396(4):511-20. PubMed PMID: 9651008.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Expression of differential immune factors in temporal cortex and cerebellum: the role of alpha-1-antichymotrypsin, apolipoprotein E, and reactive glia in the progression of Alzheimer's disease. AU - Styren,S D, AU - Kamboh,M I, AU - DeKosky,S T, PY - 1998/7/3/pubmed PY - 2000/6/20/medline PY - 1998/7/3/entrez SP - 511 EP - 20 JF - The Journal of comparative neurology JO - J. Comp. Neurol. VL - 396 IS - 4 N2 - A variety of factors and processes have been implicated in the development and progression of the pathology of Alzheimer's Disease (AD), including amyloid fragment deposition, reactive gliosis, alpha-1-antichymotrypsin (ACT), and apolipoprotein E (APOE). Carriers of the APOE 4 allele have been shown to have an enhanced risk of developing AD, and the ACT signal peptide A/A genotype may modify the APOEepsilon4 risk. The protein products of these genes have been shown to enhance conversion of diffuse beta amyloid (Abeta) fibrils, which are found in diffuse plaques, to the fibrillar form found in neuritic plaques. In affected regions of AD brain, ACT and APOE colocalize with Abeta deposits and reactive microglia and astrocytes. We examined the regional distribution of ACT, APOE, and reactive glia in temporal cortex, where neuritic plaques are abundant, and cerebellum (in areas where diffuse plaques but not neuritic plaques accumulate) to examine the relationship of these markers to the deposition of Abeta. In temporal cortex, ACT and APOE staining was localized to plaque-like profiles, reactive astrocytes, and blood vessels; human leukocyte antigen-DR (HLA-DR) and glial fibrillary acidic protein (GFAP) staining revealed focal clusters of reactive microglia and astrocytes. In cerebellum, ACT and APOE immunoreactivity was never localized to plaque-like profiles but was weakly localized to unreactive astrocytes; weak HLA-DR and GFAP immunoreactivity was present on quiescent microglia throughout the cerebellum. The lack of fibrillar amyloid deposits in cerebellum, despite the presence of well-characterized markers thought to mediate the production of Abeta, suggests that this brain region may be lacking certain factors necessary for fibril formation or that the cerebellum responds differently to stimuli that successfully mediate inflammation in affected cortex. SN - 0021-9967 UR - https://www.unboundmedicine.com/medline/citation/9651008/Expression_of_differential_immune_factors_in_temporal_cortex_and_cerebellum:_the_role_of_alpha_1_antichymotrypsin_apolipoprotein_E_and_reactive_glia_in_the_progression_of_Alzheimer's_disease_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0021-9967&date=1998&volume=396&issue=4&spage=511 DB - PRIME DP - Unbound Medicine ER -