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Peripheral-type benzodiazepine binding in Alzheimer disease
E G McGeer1, E A Singh, P L McGeer
1Kinsmen Laboratory of Neurological Research, Department of Psychiatry, University of British Columbia, Vancouver, Canada.
Alzheimer Disease and Associated Disorders
|January 1, 1988
Summary
Alzheimer disease (AD) brains show reduced choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities. However, peripheral-type benzodiazepine binding sites are significantly increased in AD cortical areas, suggesting altered neurochemistry in this neurodegenerative condition.
Area of Science:
- Neuroscience
- Neuropathology
Background:
- Alzheimer disease (AD) is characterized by neuronal loss and cholinergic deficits.
- Peripheral-type benzodiazepine binding sites (PTBS) are implicated in neuroinflammation and neuroprotection.
Purpose of the Study:
- To investigate PTBS density and cholinergic enzyme activities in postmortem brains of AD patients.
- To compare these markers between AD, age-matched controls, and other neurological conditions.
Main Methods:
- Measurement of [3H]Ro5-4864 binding and choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities.
- Analysis of 7 cortical areas from postmortem brains of 18 AD patients, 12 controls, and 15 other neurological cases.
Main Results:
- ChAT and AChE activities were significantly reduced in all cortical areas of AD brains compared to controls.
- PTBS densities were significantly higher in AD brains, particularly in Broca's area and the precentral and postcentral gyri.
- Parkinson's disease patients also showed increased PTBS density, while multi-infarct dementia patients did not.
Conclusions:
- AD brains exhibit a significant reduction in cholinergic markers alongside an upregulation of PTBS.
- Increased PTBS may reflect an inflammatory or reactive process in AD and Parkinson's disease.
- These findings highlight distinct neurochemical alterations in different neurodegenerative disorders.