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P1‐480: Influence of aggregation of vascular risk factors on neuropsychological performance and white matter lesions in early Alzheimer's disease
Author(s) -
Tay Laura,
Lim Wee Shiong,
Mark Chan Peng Chew,
Chong Mei Sian,
Sitoh Yih Yian
Publication year - 2011
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.2011.05.762
Subject(s) - vascular dementia , hyperintensity , cardiology , medicine , stroke (engine) , dementia , neuroimaging , neuropsychology , white matter , verbal fluency test , risk factor , disease , psychology , cognition , psychiatry , magnetic resonance imaging , radiology , mechanical engineering , engineering
Background:Mutations in the CHMP2B gene on chromosome 3 are a rare cause of familial FTD (FTD-3). A Danish family with FTD-3 has been followed by a multinational and multidisciplinary research group (Frontotemporal dementia Research in Jutland Association, FReJA) for more than two decades. The clinical phenotype of FTD-3 has been described with early changes in behavior and personality typical of the behavioral variant of FTD. The impression is however, that FTD-3 patients often are more globally affected than most other FTD cases [l]. Neuropsychological data on FTD-3 in the early stage has only been presented in a case report in 2002 [1] and as preliminary data in a cross-sectional study including haplotyped family members [2]. While the case study showed generalized cognitive impairment with relatively preserved episodic memory, the study of preclinical symptoms indicated predominantly frontal lobe involvement years before overt dementia symptoms. The objective of this study is to characterize neuropsychological changes in the preclinical phase of FTD-3. Methods: As part of a cross-sectional and longitudinal study, 37 FTD-3 family members aged 40 70 were assessed with neuropsychological tests in 2002, 2005 and 2010. Five subjects showed clinical signs of dementia at the last session. In order to assess the earliest neuropsychological dysfunctions in FTD-3, data from 2002 and 2005 from these five subjects are being analysed. Results: The normative data that constitute the basis for this analysis consist of data from family members known not to be CHMP2Bmutation carriers (estimated 25) and 22 spouses. The clinical investigators including the testing neuropsychologist are blind to the mutation status of the participants. Currently we still lack a few mutation analyses and the final quantitative group analysis including the 2010 assessments will be ready by April 2011. Conclusions: Neuropsychological impairments seem to be detectable 5-8 years before the clinical onset of dementia in FTD-3. Some patients show a typical dysexecutive syndrome while others seem to be more globally affected at the preclinical stage. This work is a part of the FReJA research collaboration. References: [1] Neurology 2002;59;1585-94. [2] Neurobiology of Aging 2004;25:453.