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P1‐340: FRONTOTEMPORAL DEMENTIA‐LIKE PHENOTYPE IN SEVEN HISPANIC PATIENTS WITH PRESENILIN‐2
Author(s) -
Rivera Natalie,
Ramírez Ginette González,
Rivera Alexandra,
Rodriguez María,
Nieves José,
Pérez Arturo,
Valentin Eric Miranda,
Rivera Horacio Serrano,
Canabal Jorge Acevedo,
Rivera Agosto Mariela Melissa,
Maldonado Aleyda,
Jiménez-Velázquez Ivonne Z.,
Lee Joseph H.
Publication year - 2018
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2018.06.347
Subject(s) - frontotemporal dementia , dementia , presenilin , personality changes , disease , atrophy , family history , medicine , psychiatry , pediatrics , psychology , memory clinic , alzheimer's disease
by gender and presence of Lewy bodies (LB). Results:Overall, carriers of ε4 showed a greater frequency of N+ than non-carriers (p1⁄40.017). NAD female carriers had significantly more N+, independent of the presence of LB (p1⁄40.009) (Fig 1). In HAD subjects, homozygous carriers of the ε4 allele showed a significant increase in the frequency of N+ over heterozygous or non-carriers of the ε4 allele; this significant association was present only in females, and only in thosewith LB (p1⁄40.020) (Fig 2). No significant relationship was detected in the IAD group. Conclusions:The effect of ApoE ε4 on N+ seems female predominant, and varies based on AD pathology severity. ApoE ε4 exerts a recessive-like effect on N+ in HAD females, but only in the presence of LB; this finding is similar to the recently reported effect of ε4 on psychosis (1), another common symptom of AD. Our unexpected finding that female NAD ε4 carriers show a higher prevalence of N+, an effect independent of AD pathology and LB, suggests for the possible influence of ApoE ε4 on non-AD related issues not previously recognized. Kim J, Fischer CE, Schweizer TA, Munoz DG. Gender and Pathology-Specific Effect of Apolipoprotein E Genotype on Psychosis in Alzheimer’s Disease. Curr Alzheimer Res. 2017;14(8):834-40.