Association study of brain-derived neurotrophic factor and apolipoprotein E polymorphisms and cognitive function in aged males without dementia

Tsai, Shih‐Jen; Gau, Yung‐Tian A.; Liu, Mu-En; Hsieh, Cheng-Hsi; Liou, Ying‐Jay

doi:10.1016/j.neulet.2007.12.057

Cited by 29 publications

(36 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The current sample sizes for the BDNF genotype and hippocampus analyses were larger than those in the existing literature (Ns=36–173) (Benjamin et al, 2010; Bueller et al, 2006; Frodl et al, 2007; Karnik et al, 2010; Pezawas et al, 2004; Richter-Schmidinger et al, 2011; Schofield et al, 2009; Szeszko et al, 2005), and the BDNF genotype-memory samples were similar or larger than all but one of the existing studies (Ns=28–475) (Benjamin et al, 2010; Dempster et al, 2005; Egan et al, 2003; Goldberg et al, 2008; Hariri et al, 2003; Hashimoto et al, 2008; Ho et al, 2006; Karnik et al, 2010; Kennedy et al, 2014; Raz et al, 2008 and 2009; Richter-Schmidinger et al, 2011; Schofield et al, 2009; Strauss et al, 2004; Tsai et al, 2008; Yu et al, 2008; but see Miyajima et al, 2008; N=722). In addition, the current sample sizes for the plasma BDNF and hippocampus analyses were similar or larger than in the existing literature (Ns=20–142) (Driscoll et al, 2012; Eker et al, 2010; Erickson et al, 2010; Rizos et al, 2011), and the plasma BDNF-memory cohorts were similar or larger than all but two of the existing studies (Ns=35–429) (Dias et al, 2009; Driscoll et al, 2012; Gunstad et al, 2008; Li et al, 2009; O’Bryant et al, 2010; Ruiz de Azua et al, 2013; Yu et al, 2008; but see Komulainen et al, 2008 (N=1389); Shimada et al, 2014 (N=4463).…”

Section: Discussionmentioning

confidence: 86%

“…Past studies in healthy middle-aged and older adult cohorts have also failed to find a difference for hippocampal volume (Benjamin et al, 2010; Karnik et al, 2010; Miyajima et al, 2008; but see Pezawas et al, 2004). While two past studies including middle-aged and older adult cohorts observed worse memory performance for Met carriers (Miyajima et al, 2008; Raz et al, 2009), several others failed to find significant group differences (Benjamin et al, 2010; Harris et al, 2006; Karnik et al, 2010; Raz et al, 2008; Tsai et al, 2008). Thus, incorporating current results, the preponderance of investigations suggests minimal effects of the BDNF genotype on memory performance at later age ranges.…”

Section: Discussionmentioning

confidence: 90%

“…In addition, findings have been inconsistent in regards to episodic memory performance in this age range with some observations of significantly lower performance in Met carriers (Kennedy et al, 2014; Miyajima et al, 2008; Raz, Rodrigue, Kennedy, & Land, 2009), and other reports of no significant differences between Val/Val and Met carrier groups (Benjamin et al, 2010; Harris et al, 2006; Karnik et al, 2010; Tsai et al, 2008). Previous studies have used various methods for determining hippocampal volume, including manual tracing (Bueller et al, 2006; Frodl et al, 2007; Richter-Schmidinger et al, 2011; Szeszko et al, 2005), point counting (Benjamin et al, 2010; Miyajima et al, 2008) and voxel-based morphometry (Pezawas et al, 2004; Schofield et al, 2009).…”

Section: Introductionmentioning

confidence: 94%

See 2 more Smart Citations

Lack of an association of BDNF Val66Met polymorphism and plasma BDNF with hippocampal volume and memory

Kim

Goate

Benzinger³

et al. 2015

Cogn Affect Behav Neurosci

View full text Add to dashboard Cite

Brain-derived neurotrophic factor (BDNF) has been shown to be important for neuronal survival and synaptic plasticity in the hippocampus in non-human animals. The Val66Met polymorphism in the BDNF gene, involving a valine (Val) to methionine (Met) substitution at codon 66, has been associated with lower BDNF secretion in vitro. However, there have been mixed results regarding associations between either circulating BDNF or the BDNF Val66Met polymorphism with hippocampal volume and memory in humans. The current study examined the association of BDNF genotype and plasma BDNF with hippocampal volume and memory in two large independent cohorts of middle-aged and older adults (both cognitively normal and early-stage dementia). Sample sizes ranged from 123 to 649. Measures of the BDNF genotype, plasma BDNF, MRI-based hippocampal volume and memory performance were obtained from the Knight Alzheimer Disease Research Center (ADRC) and the Alzheimer’s Disease Neuroimaging Initiative (ADNI). There were no significant differences between BDNF Met+ and Met- groups on either hippocampal volume or memory in either cohort. In addition, plasma BDNF was not significantly associated with either hippocampal volume or memory in either cohort. Neither age, cognitive status nor gender moderated any of the relationships. Overall, current findings suggest that BDNF genotype and plasma BDNF may not be robust predictors for variance in hippocampal volume and memory in middle age and older adult cohorts.

show abstract

Section: Discussionmentioning

confidence: 86%

Section: Discussionmentioning

confidence: 90%

Section: Introductionmentioning

confidence: 94%

See 1 more Smart Citation

Lack of an association of BDNF Val66Met polymorphism and plasma BDNF with hippocampal volume and memory

Kim

Goate

Benzinger³

et al. 2015

Cogn Affect Behav Neurosci

View full text Add to dashboard Cite

show abstract

“…The mechanisms for this gender-specific observation-although indirectly supported by a recent study in male failing to show an association between the Val66Met polymorphisms and cognitive function assessed by various cognitive domains (Tsai et al 2008)-remain unclear and require replication and further assessment in independent and larger samples utilising comparable cognitive phenotypes. In contrast to our finding, a larger Scottish study on cognitive aging showed an association between the Met66 allele and improved reasoning skills; however, reasoning skills describe different cognitive abilities than our cognitive phenotypes, which make the studies not directly comparable.…”

Section: Discussionmentioning

confidence: 99%

Brain-derived neurotrophic factor (BDNF) gene: a gender-specific role in cognitive function during normal cognitive aging of the MEMO-Study?

Laing

Mitchell

Wersching³

et al. 2011

AGE

View full text Add to dashboard Cite

Cognitive aging processes are underpinned by multiple processes including genetic factors. The brain-derived neurotrophic factor (BDNF) has been suggested to be involved in age-related cognitive decline in otherwise healthy individuals. The genderspecific role of the BDNF gene in cognitive aging remains unclear. The identification of genetic biomarkers might be a useful approach to identify individuals at risk of cognitive decline during healthy aging processes. The aim of this study was to investigate the associations between three singlenucleotide polymorphisms (SNPs) in the BDNF gene and domains of cognitive functioning in normal cognitive aging. The sample, comprising 369 participants (M=72.7 years, SD=4.45 years), completed an extensive neuropsychological test battery measuring memory, motor function, and perceptual speed. The relationships between the SNPs rs6265, rs7103411, and rs7124442 and cognitive domains were examined. While significant main effects of BDNF SNPs on cognitive function were found for the association between rs7103411 and memory performance, gender-specific analyses revealed for females significant main effects of rs7103411 for memory and of rs6265 for perceptual speed independent of the APOE*E4 status and education. The finding for the association between rs6265 and perceptual speed in females remained significant after Bonferroni correction for multiple comparisons. None of the analyses showed significant results for males. This study is the first to implicate that the SNPs rs6265 and rs7103411 affect cognitive function in the elderly in a genderspecific way.

show abstract

“…It has been recommended that researchers should be aiming to break the "1% quantitative trait loci barrier" which requires between 800 and 1000 samples to detect a polymorphism which accounts for at least 1% of the variance in cognitive ability within the general population with 80% power (Plomin 2003;Craig and Plomin 2006). Unfortunately, as can be seen in Tables 1, 2, 3, 4 and 5 only a small proportion of cognitive genetic research groups reach or break this threshold and even some recent studies still seem content to use sample sizes of a few hundred or less (Bombin et al 2008;Tsai et al 2008;Izumi et al 2008; Brain-derived neurotrophic factor (BDNF); RE1-silencing transcription factor (REST); cathepsin D (CTSD); apolipoprotein E (APOE); major histocompatibility complex, class II, DR beta 1 (HLA-DRB1); prion protein (PRPN); klotho (KL); cholinergic receptor, nicotinic, alpha 4 (CHRNA4); cholinergic receptor, muscarinic 2 (CHRM2); dopamine receptor D4 (DRD4); fatty acid desaturase 2 (FADS2); glutathione S-transferase pi 1 (GSTP1); hemochromatosis (HFE); 5,10-methylenetetrahydrofolate reductase (MTHFR); peroxisome proliferator-activated receptor gamma (PPARG) Schaper et al 2008;Nacmias et al 2008). A further emphasis for the need of adequate sample size comes from the GWAS studies of general intelligence (Butcher et al 2005;Meaburn et al 2008;Butcher et al 2008).…”

Section: Sample Sizementioning

confidence: 99%

The Impact of Genetic Research on our Understanding of Normal Cognitive Ageing: 1995 to 2009

Payton

2009

Neuropsychol Rev

View full text Add to dashboard Cite

Identifying the risk factors for individual differences in age-related cognitive ability and decline is amongst the greatest challenges facing the healthcare of older people. Cognitive impairment caused by "normal ageing" is a major contributor towards overall cognitive deficit in the elderly and a process that exhibits substantial inter- and intra-individual differences. Both cognitive ability and its decline with age are influenced by genetic variation that may act independently or via epistasis/gene-environment interaction. Over the past fourteen years genetic research has aimed to identify the polymorphisms responsible for high cognitive functioning and successful cognitive ageing. Unfortunately, during this period a bewildering array of contrasting reports have appeared in the literature that have implicated over 50 genes with effect sizes ranging from 0.1 to 21%. This review will provide a comprehensive account of the studies performed on cognitively healthy individuals, from the first study conducted in 1995 to present. Based on current knowledge the strong and weak methodologies will be identified and suggestions for future study design will be presented.

show abstract

Association study of brain-derived neurotrophic factor and apolipoprotein E polymorphisms and cognitive function in aged males without dementia

Cited by 29 publications

References 38 publications

Lack of an association of BDNF Val66Met polymorphism and plasma BDNF with hippocampal volume and memory

Lack of an association of BDNF Val66Met polymorphism and plasma BDNF with hippocampal volume and memory

Brain-derived neurotrophic factor (BDNF) gene: a gender-specific role in cognitive function during normal cognitive aging of the MEMO-Study?

The Impact of Genetic Research on our Understanding of Normal Cognitive Ageing: 1995 to 2009

Contact Info

Product

Resources

About