Kurzfassung

Alzheimer's disease (AD) is characterized by amyloid ß (Aß)-deposition in amyloid plaques, neurofibrillary tangles, glial activation, selective neuronal loss and cognitive deficits. Cannabinoids have been shown to display neuroprotective effects in a variety of neurodegenerative paradigms and to affect neuronal plasticity and memory. They exert their effects by binding to membrane cannabinoid receptors, CB1 and CB2. Examination of brain samples from AD patients revealed a reduced number of...
Alzheimer's disease (AD) is characterized by amyloid ß (Aß)-deposition in amyloid plaques, neurofibrillary tangles, glial activation, selective neuronal loss and cognitive deficits. Cannabinoids have been shown to display neuroprotective effects in a variety of neurodegenerative paradigms and to affect neuronal plasticity and memory. They exert their effects by binding to membrane cannabinoid receptors, CB1 and CB2. Examination of brain samples from AD patients revealed a reduced number of CB1-expressing neuronal cells in brain areas affected by amyloid plaque deposition and microglial activation. Injection of cannabinoids in A-treated rats prevented glial activation, neuronal loss and cognitive deficits. This background prompted us to study the involvement of the endogenous cannabinoid system in the development of AD by breeding APP23 mice, a well described AD transgenic mouse model, with CB1-deficient mice. We plan to examine brains of these mice for AD typical amyloid plaques and microglial activation and to test animals for their learning and memory capabilities. These studies will be complemented by in vitro experiments studying the effects of cannabinoids on amyloid precursor protein (APP)-processing that gives rise to the toxic Aß-peptide.

extern begutachtetes Forschungsprojekt


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