BDNF Val66Met Polymorphism Interacts with Sleep Consolidation to Predict Ability to Create New Declarative Memories

Gosselin, Nadia; Beaumont, Louis De; Gagnon, Katia; Baril, Andrée‐Ann; Mongrain, Valérie; Blais, Hélène; Montplaisir, J; Gagnon, Jean‐François; Pelleïeux, Sandra; Poirier, Judes; Carrier, Julie

doi:10.1523/jneurosci.4432-15.2016

Cited by 31 publications

(34 citation statements)

References 55 publications

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“…Although we did not find any interactions of sleep with BDNF genotype in this cancer survivor cohort, this genotype has been shown to interact with sleep in effects on cognition in patients without cancer. Taken together, our results suggest that sleep may be particularly important for memory among cancer survivors with polymorphisms that are known to increase the risk of dementias . Future exploration of a wider array of genotypes could advance our knowledge about mechanisms of cancer‐related cognitive decline.…”

Section: Discussionmentioning

confidence: 63%

“…Taken together, our results suggest that sleep may be particularly important for memory among cancer survivors with polymorphisms that are known to increase the risk of dementias. 15 Future exploration of a wider array of genotypes could advance our knowledge about mechanisms of cancer-related cognitive decline.…”

Section: Discussionmentioning

confidence: 99%

“…Prior research has proposed that these genetic variants increase the risk for cognitive decline in general populations and in cancer survivors after treatment and that specific vulnerability factors may interact in accelerating this risk (ie, a gene‐environment interaction) . One salient factor that could influence this risk is poor sleep . Despite these links, limited research has tested the interaction of genotype with sleep disturbance in predicting risk for cognitive decline, with no research to date testing these relationships in cancer survivors.…”

Section: Introductionmentioning

confidence: 99%

“…[4][5][6] Sleep disturbance has been identified as a risk factor for the development of cognitive decline and Alzheimer disease (AD) in noncancer populations. [7][8][9][10] Likewise, a number of genetic vulnerabilities for cognitive decline in later life, including variants in the APOE, 11,12 COMT, 13,14 and BDNF genes, [15][16][17] have been identified. Prior research has proposed that these genetic variants increase the risk for cognitive decline in general populations and in cancer survivors after treatment and that specific vulnerability factors may interact in accelerating this risk (ie, a gene-environment interaction).…”

Section: Introductionmentioning

confidence: 99%

“…12,14 One salient factor that could influence this risk is poor sleep. 15,18 Despite these links, limited research has tested the Cancer December 15, 2019 interaction of genotype with sleep disturbance in predicting risk for cognitive decline, 15,18 with no research to date testing these relationships in cancer survivors. Indeed, the contribution of sleep to cognitive declines and genetic vulnerability among cancer survivors remains relatively unexplored despite the observation that sleep disturbance is highly prevalent among cancer survivors, with the incidence of insomnia in cancer survivors 2-to 3-fold greater than rates among similarly aged controls.…”

Section: Introductionmentioning

confidence: 99%

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Sleep disturbance and neurocognitive outcomes in older patients with breast cancer: Interaction with genotype

Carroll¹,

Small

Tometich

et al. 2019

Cancer

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Background Sleep disturbance and genetic profile are risks for cognitive decline in noncancer populations, yet their role in cancer‐related cognitive problems remains understudied. This study examined whether sleep disturbance was associated with worse neurocognitive outcomes in breast cancer survivors and whether sleep effects on cognition varied by genotype. Methods Newly diagnosed female patients (n = 319) who were 60 years old or older and had stage 0 to III breast cancer were recruited from August 2010 to December 2015. Assessments were performed before systemic therapy and 12 and 24 months later. Neuropsychological testing measured attention, processing speed, executive function, learning, and memory; self‐perceived cognitive functioning was also assessed. Sleep disturbance was defined by self‐report of routine poor or restless sleep. Genotyping included APOE, BDNF, and COMT polymorphisms. Random effects fluctuation models tested associations of between‐person and within‐person differences in sleep, genotype, and sleep‐genotype interactions and cognition and controlled for age, reading level, race, site, and treatment. Results One‐third of the patients reported sleep disturbances at each time point. There was a sleep‐APOE ε4 interaction (P = .001) in which patients with the APOE ε4 allele and sleep disturbances had significantly lower learning and memory scores than those who were APOE ε4‐negative and without sleep disturbances. There was also a sleep disturbance–COMT genotype interaction (P = .02) in which COMT Val carriers with sleep disturbances had lower perceived cognition than noncarriers. Conclusions Sleep disturbance was common and was associated with worse cognitive performance in older breast cancer survivors, especially those with a genetic risk for cognitive decline. Survivorship care should include sleep assessments and interventions to address sleep problems.

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Section: Discussionmentioning

confidence: 63%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Sleep disturbance and neurocognitive outcomes in older patients with breast cancer: Interaction with genotype

Carroll¹,

Small

Tometich

et al. 2019

Cancer

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Proximity to Parental Symptom Onset and Amyloid-β Burden in Sporadic Alzheimer Disease

et al. 2018

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IMPORTANCE Alzheimer disease (AD) develops during several decades. Presymptomatic individuals might be the best candidates for clinical trials, but their identification is challenging because they have no symptoms. OBJECTIVE To assess whether a sporadic parental estimated years to symptom onset calculation could be used to identify information about amyloid-β (Aβ) levels in asymptomatic individuals with a parental history of AD dementia. DESIGN, SETTING, AND PARTICIPANTS This cohort study analyzed Aβ1-42 in cerebrospinal fluid (CSF) specimens from 101 cognitively normal individuals who had a lumbar puncture as part of the Presymptomatic Evaluation of Novel or Experimental Treatments for Alzheimer Disease (PREVENT-AD) cohort from September 1, 2011, through November 30, 2016 (374 participants were enrolled in the cohort during this period). The study estimated each participant's proximity to his/her parent's symptom onset by subtracting the index relative's onset age from his/her current age. The association between proximity to parental symptom onset and Aβ levels was then assessed using apolipoprotein E ε4 (APOE4) status and sex as interactive terms. These analyses were performed again in 2 independent cohorts using CSF and Pittsburgh compound B carbon 11-labeled positron emission tomography (PIB-PET) Aβ biomarkers: the Adult Children Study (ACS) and the Wisconsin Registry for Alzheimer Prevention (WRAP) cohorts. MAIN OUTCOMES AND MEASURES The association between proximity to parental symptom onset and Aβ burden in asymptomatic individuals with a parental history of sporadic AD. RESULTS The present analysis included a subset of 101 PREVENT-AD individuals (mean [SD] age, 61.8 [5.1] years; 30 [29.7%] male), 128 ACS participants (112 participants underwent CSF measurement: mean [SD] age, 63.4 [5.1] years; 31 [27.7%] male; and 107 underwent PIB-PET: mean [SD] age, 64.6 [5.3] years; 27 [25.2%] male), and 135 WRAP participants (85 participants underwent CSF measurement: mean [SD] age, 59.9 [6.0] years; 27 [31.8%] male; and 135 underwent PIB-PET: mean [SD] age, 59.6 [6.1] years; 43 [31.9%] male). In the PREVENT-AD cohort, individuals approaching their parent's onset age had lower CSF Aβ1-42 levels (range, 402-1597; B = −9.09, P = .04). This association was stronger in APOE4 carriers (B = −17.9, P = .03) and women (B = −19.8, P = .02). In the ACS cohort, the main association was replicated using PIB-PET data, and the sex interaction was replicated using CSF and PIB-PET data. In the WRAP cohort, the results were not replicated using cross-sectional data, but the main association and the APOE interaction were replicated using PIB-PET longitudinal data. CONCLUSIONS AND RELEVANCE These results suggest that proximity to parental symptom onset may help estimate Aβ biomarker changes in women or APOE4 carrier asymptomatic individuals with a parental history of sporadic AD.

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Open science datasets from PREVENT‐AD, a longitudinal cohort of pre‐symptomatic Alzheimer’s disease

Tremblay‐Mercier

Binette

Madjar

et al. 2021

Alzheimer's & Dementia

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Background: In the last 10 years, the PResymptomatic EValuation of Experimental or Novel Treatments for Alzheimer Disease (PREVENT-AD) research program has collected both biological and behavioral data longitudinally, using well-recognized biomarkers, to better understand and prevent Alzheimer's disease (AD). Our cohort is composed of older individuals with a family history of AD, but who were themselves cognitively unimpaired when enrolled in the study (aged 63 years old ± 5, at entry). To move AD research further, we recently shared this rich dataset with the global research community. Method:We created a data sharing model including two levels of access based on data sensitivity and risk of potential re-identification, framed with a series of usage terms.Preparation of the datasets included selection of the variables to share, quality controls, outlier analysis, de-identification, and creation of detailed data dictionaries for proper re-usability. Each research participant was retrospectively re-consented.Result: More than 90% of participants (349 out of 386) agreed to openly share their data. Repositories are accessible openly at https://openpreventad.loris.ca, to qualified researchers at https://registeredpreventad.loris.ca, and through the unified interface of the Canadian Open Neuroscience Platform. The shared data collected from 2012 to 2020 (Table 1) includes longitudinal multimodal magnetic resonance imaging, gene variants, neuropsychological assessments, neurosensory evaluations, subjective cognitive decline information, as well as multiple behavioral data (e.g. sleep quality, neuropsychiatric factors, personality traits, etc). Amyloid and tau measurements from cerebrospinal fluid (n=106; longitudinal) and positron emission tomography (n = 130) are also available on subsamples of participants. To date, more than 250 users have accessed the PREVENT-AD datasets. Conclusion:Creation of open datasets from sensitive human data requires technical, human, and financial investments. The challenge remains important as we must con-

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BDNF Val66Met Polymorphism Interacts with Sleep Consolidation to Predict Ability to Create New Declarative Memories

Cited by 31 publications

References 55 publications

Sleep disturbance and neurocognitive outcomes in older patients with breast cancer: Interaction with genotype

Sleep disturbance and neurocognitive outcomes in older patients with breast cancer: Interaction with genotype

Proximity to Parental Symptom Onset and Amyloid-β Burden in Sporadic Alzheimer Disease

Open science datasets from PREVENT‐AD, a longitudinal cohort of pre‐symptomatic Alzheimer’s disease

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