AI Article Synopsis

  • The study explores cholinergic dysfunction in Alzheimer's disease, focusing on the loss of magnocellular cholinergic neurons in the basal nucleus of Meynert.
  • Rats with lesions in the basal nucleus exhibit learning and memory issues, leading researchers to assess nicotinic acetylcholine receptor alpha4 protein expression in their frontal cortex.
  • Results show a significant increase in alpha4 expression one week after lesioning, but no differences after four weeks, suggesting that basal nucleus lesions may not effectively model Alzheimer's disease as they typically show decreased receptor expression.

Article Abstract

An important feature of cholinergic dysfunction in Alzheimer's disease (AD) is the degenerative loss of magnocellular cholinergic neurons in the basal nucleus of Meynert. In search for suitable animal models of Alzheimer dementia, rats with lesioned basal nuclei rats have been shown to display learning and memory disturbances. We here report on the quantitative assessment of the expression of the nicotinic acetylcholine receptor alpha4 protein in the rat frontal cerebral cortex following a unilateral lesion of the basal nucleus. Cortical alpha4 isoform expression shows a significant increase on the lesioned vs. the non-lesioned control side 1 week after lesioning. By contrast, no differences were observed 4 weeks after lesioning. In consideration of these results basal nucleus lesions appear as a questionable model of AD which in contrast to the present findings shows a decrease of cortical alpha4 nicotinic acetylcholine receptor protein expression.

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Source
http://dx.doi.org/10.1016/s0304-3940(01)01605-6DOI Listing

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