Abstract
The decline of cognitive function associated with aging is thought to involve deficits in brain cholinergic mechanisms (4, 8, 16, 21, 28). Cognitive deterioration is greatly exacerbated in senile dementia of the Alzheimer’s type (SDAT). In this disease the activity of choline acetyltransferase (ChAT), the synthetic enzyme for acetylcholine (ACh), is markedly reduced in cortex and hippocampus, when compared to age-matched controls (5, 8, 22, 25, 26). The decrease of ChAT activity in cortex is closely correlated with the severity of cognitive impairment and the extent of neuropathology (5, 22). High affinity uptake of choline (Ch) and in vitro synthesis of ACh in cortical tissue biopsied from SDAT patients were reduced (29, 30). These biochemical changes in Alzheimer’s patients appear to reflect a loss of cholinergic innervation to hippocampus and cortex (31, 34), which subserve an important role in memory and cognition (4, 11). Therefore, many of the recent strategies for treatment of SDAT reflect attempts to reverse this deficit in cholinergic function.
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Sherman, K.A., Friedman, E. (1986). Human Red Blood Cell Choline in Aging and Senile Dementia: Effects of Precursor Therapy. In: Hanin, I. (eds) Dynamics of Cholinergic Function. Advances in Behavioral Biology, vol 30. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5194-8_27
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DOI: https://doi.org/10.1007/978-1-4684-5194-8_27
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