Nicastrin gene polymorphisms, cognitive ability level and cognitive ageing
Section snippets
Acknowledgements
The authors thank the Biotechnology and Biological Sciences Research Council for support. We thank Martha Whiteman and Alison Pattie for gathering phenotype data. Ian Deary is the recipient of a Royal Society-Wolfson Research Merit Award. Lawrence Whalley holds a Wellcome Trust Career Development Award.
References (28)
- et al.
Mild cognitive impairment in older people
Lancet
(2002) - et al.
No replication between the Nicastrin gene and familial early-onset Alzheimer's disease
Neurosci. Lett.
(2003) - et al.
Searching for genetic influences on normal cognitive ageing
Trends Cogn. Sci.
(2004) Mild cognitive impairment: prevalence, prognosis, aetiology, and treatment
Lancet Neurol.
(2003)Aph-1, Pen-2, and Nicastrin with Presenilin generate an active g-secretase complex
Neuron
(2003)- et al.
Achieving and maintaining cognitive vitality with aging
Mayo Clin. Proc.
(2002) - et al.
‘Mini Mental State’: a practical method for grading the cognitive state of patients for the clinician
J. Psychiatr. Res.
(1975) Apolipoproteins and aging: emerging mechanisms
Ageing Res. Rev.
(2002)- et al.
Results of a high-resolution genome screen of 437 Alzheimer disease families
Hum. Mol. Genet.
(2003) - et al.
Genetic and environmental influences on human psychological differences
J. Neurobiol.
(2003)
Cognitive change and the APOE e4 allele
Nature
Apolipoprotien E gene variability and cognitive functions at age 79: follow up of the Scottish Mental Survey 1932
Psychol. Aging
The impact of childhood intelligence on later life: following up the Scottish Mental Surveys of 1932 and 1947
J. Pers. Soc. Psychol.
Am. J. Hum. Genet.
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Nicastrin Deficiency Induces Tyrosinase-Dependent Depigmentation and Skin Inflammation
2020, Journal of Investigative DermatologyCitation Excerpt :Nonetheless, there are controversial studies showing that γ-secretase substrates could still be processed without Nicastrin (Hu et al., 2015; Zhao et al., 2010), suggesting that the requirement of Nicastrin could vary from cells to cells. So far, altered expression, mutations or polymorphisms in nicastrin have been associated with the occurrence of inflammatory acne inversa (Wang et al., 2010), life-long cognitive ability (Deary et al., 2005), and neurodegeneration (Tabuchi et al., 2009; Zhong et al., 2009). Here we show that nicastrin deficiency in the zebrafish embryos leads to curled-up tail, depigmentation with ruptured melanosomes, swollen mitochondria, necrotic-like nuclei, and non-apoptotic death of melanophores, the fish counterparts of melanocytes.
A dopamine receptor genetic variant enhances perceptual speed in cognitive healthy subjects
2017, Alzheimer's and Dementia: Translational Research and Clinical InterventionsCitation Excerpt :Results from a meta-analysis of 23 independent twin studies also showed that heritability estimates vary across the different specific domains [3]. Several studies have reported genetic associations with a priori biological relevant genes for cognition; however, results have not been consistently replicated [4–13]. Genetic-agnostic approaches through genome-wide association analysis (GWAS) have also been reported for different cognitive tasks [14–21].
Genetics of human memory functions in healthy cohorts
2015, Current Opinion in Behavioral SciencesFunctional and genetic analysis of haplotypic sequence variation at the nicastrin genomic locus
2012, Neurobiology of AgingCitation Excerpt :Four main haplotypes have been identified at the NCSTN locus; HapA, HapB, HapC, and HapD (Dermaut et al., 2002). In addition, we have previously defined a further haplotype, HapE (Deary et al., 2005). Of these, HapB was shown to increase risk of developing familial early onset Alzheimer's disease in Dutch individuals, particularly those without an APOE ε4 allele (Dermaut et al., 2002).
Association of KIBRA and memory
2009, Neuroscience LettersCOMT genotype and cognitive ability: A longitudinal aging study
2007, Neuroscience Letters