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Conclusion

Dementia is more frequently observed in autosomal dominant forms of PD (particularly in cases caused by SNCA mutation) than in the recessive forms. The genetic basis of dementia occurring in apparently sporadic PD is less well understood, with variability in APOE and GBA being the most consistent genetic risk factors. The primary goal of disease genetics is to shed light onto the molecular aetiology of disease with an eye toward defining potential points for therapeutic intervention. Clearly there has been substantial progress in the genetics of PD (and implicitly PD-D); however, there is still a long way to go. The tools are now at hand to achieve a more complete understanding of the genetic basis of common complex diseases, including PD-D. Not only will a more complete genetic understanding of these diseases inform us about aetiology, but it is also likely to add more clarity to the idea that this disease is aetiologically similar to DLB and AD. There will certainly be challenges to a successful dissection of the genetic basis of PD-D, perhaps the most immediate of which is that of achieving sufficient sample size to detect and confirm a genuine genetic association; however, for the first time the route to success is relatively clear.

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