Behavioral and Psychological Symptoms in Dementia (BPSD), especially psychotic symptoms, are particularly frequent in patients with Dementia with Lewy bodies. Several studies, focussing predominantly upon the cholinergic system, have evaluated the potential neurochemical associations of these symptoms. Visual hallucinations appear to be associated with reduced cortical choline acetyltransferase (ChAT) activity in the temporal cortex, a marker of cholinergic innervation, but not with predominantly postsynaptic muscarinic M1 receptor binding; wheras delusions were significantly associated with elevated M1 receptor binding but not with reductions in ChAT. Visual hallucinations and delusional misidentification (but not delusions) were also associated associated with lower binding to nicotinic receptors ([(125)I]alpha bungarotoxin binding was reduced in the same area of the temporal cortex). No associations were identified between dopaminergic binding and any of the psychotic symptoms. In Alzheimer’s disease the relationship of psychosis to cholinergic function has not been determined, although several studies have evaluated potential associations between psychosis and nor-adrenaline, with contradictory results. There is also one report indicating a possible association between psychosis and reduced levels of serotonin in the prosubiculum. The relationship of cholinergic function to restlessness and aggression in AD has been studied, with an indication that lowered ChAT activity in the frontal and temporal cortices correlates with increasing overactivity in patients with dementia and the ratio of cholinergic to dopaminergic function appears to be associated with aggression. Whilst there are too few studies to establish a general consensus, the association of visual hallucinations with cholinergic deficts in DLB has been replicated and is consistent with the good response of visual hallucinations to cholinesterase inhibitors in these patients. The basis of BPSD symptoms may well be different in DLB and AD, and specific symptoms appear to have a different neurochemical association. Further studies are urgently needed in order to facilitate a meaningful treatment approach to the treatment of BPSD in people with dementia.
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