Apolipoprotein E e4 allele frequency in patients with multiple system atrophy
Section snippets
Acknowledgements
We would like to thank Mrs. Linda Elliott and Mr. Paul Carter for technical help with the preparation of the tissue and Mrs. Sandra Randell for secretarial assistance. This work was supported by the Medical Research Council, the Royal Society (N.J.C.), and the Parkinson"s Disease Society of the United Kingdom.
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2019, NeuronCitation Excerpt :Despite this strong link to DLB, APOE has not clearly been associated with other synucleinopathies such as multiple system atrophy (MSA) or Parkinson’s disease (PD). MSA is relatively rare, and to date studies examining a link between APOE and disease risk or age at onset have been negative (Cairns et al., 1997; Morris et al., 2000, 2001). In PD, an earlier meta-analysis suggested that APOE2 may be associated with increased risk (Huang et al., 2004a), but subsequent work further updated this meta-analysis and suggested that no clear significant associations could be determined (Williams-Gray et al., 2009).
The Importance of Olfactory and Motor Endpoints for Zebrafish Models of Neurodegenerative Disease
2017, Animal Models for the Study of Human Disease: Second EditionThe Importance of Olfactory and Motor Endpoints for Zebrafish Models of Neurodegenerative Disease
2013, Animal Models for the Study of Human DiseaseGenetic players in multiple system atrophy: Unfolding the nature of the beast
2011, Neurobiology of AgingCitation Excerpt :This is so far the only report on a MSA patient with abnormalities in the ZNF9 gene. Likewise, apolipoprotein E (APOE), associated with Alzheimer's disease (AD) and DLB, is not considered to be a player in MSA pathogenesis and does not contribute to an earlier disease onset (Cairns et al., 1997; Morris et al., 2000, 2001). No disease association has furthermore been detected for genetic variants of the progranulin (PRGN) gene (Yu et al., 2010).
Etiology, Pathology, and Pathogenesis
2010, Blue Books of NeurologyCitation Excerpt :The reported association between alcohol dehydrogenase 1C gene stop mutation and MSA in a British population, but not in a German population, needs further substantiation.28 The apolipoprotein E e4 allele frequency of MSA cases was not significantly different from that of control subjects.29 Similarly, others have reported no effect of apolipoprotein E tau, α-synuclein, or synphilin gene variability on the development of MSA.21,30
Chapter 3 Multiple System Atrophy
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