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Neurological Review | Sep 2012

The Genetics of Dementia With Lewy Bodies: What Are We Missing?

Bram Meeus, MSc; Jessie Theuns, PhD; Christine Van Broeckhoven, PhD, DSc

Arch Neurol. 2012;69(9):1113-1118. doi:10.1001/archneurol.2011.3678.

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ABSTRACT

Dementia with Lewy bodies is a complex brain disorder and a key member of the Lewy body disease spectrum. Its genetic etiology is unclear, and information is scattered. However, the results of molecular genetic studies imply a genetic and mechanistic overlap with Alzheimer disease, Parkinson disease with dementia, and Parkinson disease. In this review, we provide a comprehensive overview of the current studies on dementia with Lewy bodies heritability, genetic etiology, and genetic heterogeneity. We conclude with a critical discussion of the missing heritability in dementia with Lewy bodies and encourage scientists to further explore the underlying mechanisms of this disease.

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Figure 1. Clinical, neuropathological, and genetic Lewy body disease spectrum. AD indicates Alzheimer disease; DLB, dementia with Lewy bodies; and PDD, Parkinson disease with dementia.

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Figure 2. Amyloid precursor protein β-amyloid encoding region. Residues affected by mutations associated with Lewy body pathology are filled in red. ASID indicates α-secretase inhibitory domain; CTF, C-terminal fragment; Ex, exon; and NTF, N-terminal fragment. From the Alzheimer Disease & Frontotemporal Dementia Mutation Database (http://www.molgen.ua.ac.be/admutations).

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Figure 3. Presenilin proteins. The full protein sequence of PSEN1 is shown. The corresponding PSEN2 protein sequence is indicated by the orange lines. Residues affected by mutations associated with Lewy body pathology are filled in red. CTF indicates C-terminal fragment; Ex, exon; NTF, N-terminal fragment; and TM, transmembrane domain. From the Alzheimer Disease & Frontotemporal Dementia Mutation Database (http://www.molgen.ua.ac.be/admutations).

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Meeus B, Theuns J, Van Broeckhoven C. The Genetics of Dementia With Lewy Bodies: What Are We Missing?. Arch Neurol. 2012;69(9):1113-1118. doi:10.1001/archneurol.2011.3678.

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