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Conclusion

The best documented neurotransmitter changes in PD-D include loss of cholinergic markers and the progressive loss of dopamine. These deficits are associated with various changes in the related pre- and post-synaptic receptors. Alterations in serotonin, noradrenaline, and to lesser extent in other neurotransmitter systems have been reported; these are, however, less pronounced and need to be better elucidated. Neuropsychiatric and cognitive symptoms in PD-D are likely to be due to a combination of neurotransmitter deficits—particularly cholinergic and dopaminergic for cognitive dysfunction [131] (possibly with some noradrenergic influence); dopaminergic, noradrenergic, and serotonergic for depression [132]; and dopaminergic/serotonergic and cholinergic for visual hallucinations [51]. More generally there are emerging changes in synaptic machinery evident in PD-D that may also contribute to cognitive and behavioural symptoms. Clinical trials with treatment modalities such as mixed transmitter reuptake inhibitors for symptoms including depression and psychosis in PD-D are warranted [132, 133]. New possibilities for treatment targeting calcium channels [117] and perhaps synaptic dysfunction in general are also emerging.

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