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Alzheimer's disease is associated with a selective increase in α7 nicotinic acetylcholine receptor immunoreactivity in astrocytes
Author(s) -
Teaktong Thanasak,
Graham Alison,
Court Jennifer,
Perry Robert,
Jaros Evelyn,
Johnson Mary,
Hall Ros,
Perry Elaine
Publication year - 2002
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.10132
Subject(s) - nicotinic agonist , cholinergic , biology , hippocampus , acetylcholine receptor , alzheimer's disease , astrocyte , neuroscience , nicotinic acetylcholine receptor , senile plaques , acetylcholine , entorhinal cortex , endocrinology , receptor , medicine , central nervous system , disease , biochemistry
Alzheimer's disease (AD) and dementia with Lewy bodies (DLB) are common forms of dementia in the elderly associated with cholinergic dysfunction, including reductions in nicotinic acetylcholine receptors (nAChRs). In AD, astrocytes are implicated in the formation of senile plaques, one of the core pathological features. Using immunohistochemistry, we have investigated astrocytic expression of the two major nicotinic receptor α subunits in the human hippocampus and entorhinal cortex. α7, but not α4, subunit immunoreactivity was associated with astrocytes. An increase in the proportion of astrocytes expressing α7 immunoreactivity was observed in AD compared with age‐matched controls. A similar increase was not evident in DLB. Elevated α7 nAChRs on astrocytes in AD may contribute to alterations in calcium homeostasis and nitric oxide production, which in turn could affect β‐amyloid–mediated inflammatory processes in AD. GLIA 41:207–211, 2003. © 2002 Wiley‐Liss, Inc.