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Compared to a decade ago, is there better understanding of the pathophysiology of Parkinson’s disease and DLB?

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Compared to a decade ago, is there better understanding of the pathophysiology of Parkinson’s disease and DLB?

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There has been some evolution in terms of understanding. One change to highlight over the past 10 years is that the neurotransmitter deficits really are beyond dopamine in Parkinson’s disease. The noradrenergic deficits are probably as significant or close to as significant as the dopaminergic deficits. In addition, serotonergic deficits can be prominent in the illness. However, it appears that all of the brain stem monoamines are affected to some degree in Parkinson’s disease, so it really is more than just a dopamine disorder. Another prominent neurotransmitter deficit is in acetylcholine. The cholinergic deficits in Parkinson’s disease dementia are greater than in Alzheimer’s disease. Even non-demented Parkinson’s disease patients have significant cholinergic loss, so that probably helps explain the high frequency of cognitive impairments in Parkinson’s disease.

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