Cognitive Decline In Women Research Articles

Cardiovascular disease and cognitive decline in postmenopausal women: results from the Women's Health Initiative Memory Study.

BackgroundData on cardiovascular diseases (CVD) and cognitive decline are conflicting. Our objective was to investigate if CVD is associated with an increased risk for cognitive decline and to examine whether hypertension, diabetes, or adiposity modify the effect of CVD on cognitive functioning.Methods and ResultsProspective follow‐up of 6455 cognitively intact, postmenopausal women aged 65 to 79 years old enrolled in the Women's Health Initiative Memory Study (WHIMS). CVD was determined by self‐report. For cognitive decline, we assessed the incidence of mild cognitive impairment (MCI) or probable dementia (PD) via modified mini‐mental state examination (3 MS) score, neurocognitive, and neuropsychiatric examinations. The median follow‐up was 8.4 years. Women with CVD tended to be at increased risk for cognitive decline compared with those free of CVD (hazard ratio [HR], 1.29; 95% CI: 1.00, 1.67). Women with myocardial infarction or other vascular disease were at highest risk (HR, 2.10; 95% CI: 1.40, 3.15 or HR, 1.97; 95% CI: 1.34, 2.87). Angina pectoris was moderately associated with cognitive decline (HR 1.45; 95% CI: 1.05, 2.01) whereas no significant relationships were found for atrial fibrillation or heart failure. Hypertension and diabetes increased the risk for cognitive decline in women without CVD. Diabetes tended to elevate the risk for MCI/PD in women with CVD. No significant trend was seen for adiposity.ConclusionsCVD is associated with cognitive decline in elderly postmenopausal women. Hypertension and diabetes, but not adiposity, are associated with a higher risk for cognitive decline. More research is warranted on the potential of CVD prevention for preserving cognitive functioning.

Connecting Cardiovascular Disease and Dementia: Further Evidence

Cognitive impairment is highly prevalent in the elderly, and it accounts for a large part of the burden of disability and of the use of healthcare resources. The major types of dementia are Alzheimer disease and vascular dementia.[1][1] For many years, atherosclerosis was not considered to play a

Mediterranean Diet and Cognitive Decline in Women with Cardiovascular Disease or Risk Factors

BackgroundCardiovascular disease and vascular risk factors increase rates of cognitive impairment, but very little is known regarding prevention in this high-risk group. The heart-healthy Mediterranean-type dietary pattern may beneficially influence both vascular and cognitive outcomes. ObjectivesWe examined the association between Mediterranean-style diet and cognitive decline in women with prevalent vascular disease or ≥3 coronary risk factors. Design/participants/settingProspective cohort study among 2,504 women participants in the Women's Antioxidant Cardiovascular Study (WACS), a cohort of female health professionals. Adherence to a Mediterranean-style diet was determined at WACS baseline (1995-1996) using a 0- to 9-point scale with higher scores indicating higher adherence. In 1998-2000, participants aged ≥65 years underwent a telephone cognitive battery including five tests of global cognition, verbal memory, and category fluency. Tests were administered three additional times across 5.4 years. Statistical analyses performedWe used multivariable-adjusted generalized linear models for repeated measures to compare the annual rates of cognitive score changes across tertiles of Mediterranean diet score, as assessed at WACS baseline. ResultsIn both basic- and multivariable-adjusted models, consuming a Mediterranean-style diet was not related to cognitive decline. No effect modification was detected by age, education, depression, cardiovascular disease severity at WACS baseline, or level of cognition at initial assessment. ConclusionsIn women at higher risk of cognitive decline due to vascular disease or risk factors, adherence to a Mediterranean-style diet was not associated with subsequent 5-year cognitive change.

Kidney Dysfunction and Cognitive Decline in Women

ESRD is associated with substantial cognitive deficits but whether earlier kidney dysfunction predicts cognitive decline is less well defined. More than 1700 women aged ≥70 years in the Nurses' Health Study had plasma creatinine and urinary albumin/creatinine ratios (ACRs) measured in 2000, within 12 months of their initial cognitive testing. These participants had repeated assessments of cognition administered by phone every 2 years, including tests for general cognition, verbal memory, verbal fluency, and working memory for up to 6 years of follow-up. Mixed-effects regression analysis was applied to calculate mean differences in the rate of cognitive decline between women with an estimated GFR <60 ml/min per 1.73 m(2) or an ACR ≥5 mg/g versus referent levels. The median age was 74 years at initial cognitive testing, 99% of women were Caucasian, median plasma creatinine was 0.8 mg/dl, and 25% had an ACR ≥5 mg/g. The difference in cognitive decline with a baseline ACR ≥5 mg/g versus an ACR <5 mg/g was equivalent to the difference observed with 2-7 years of aging; that is, a higher ACR was associated with 2-7 times faster decline in all four cognitive domains assessed (all P values <0.05) than that attributed to each 1 year of aging alone. No associations were observed between an eGFR <60 ml/min per 1.73 m(2) and cognitive decline. A baseline urinary ACR ≥5 mg/g, a level not traditionally considered clinically significant, is independently associated with faster decline in cognitive function.

Does low-dose acetylsalicylic acid prevent cognitive decline in women with high cardiovascular risk? A 5-year follow-up of a non-demented population-based cohort of Swedish elderly women

ObjectiveThe aim of this study was to examine whether low-dose acetylsalicylic acid (ASA) influences the rate of cognitive change in elderly women.DesignProspective, population-based cohort study.SettingThe city of Gothenburg, Sweden, including...

Body &amp; brain: Apnea linked to later dementia: Sleep disorder may cause cognitive decline in women

Science NewsVolume 180, Issue 6 p. 16-16 In the News Body & brain: Apnea linked to later dementia: Sleep disorder may cause cognitive decline in women Nathan Seppa, Nathan SeppaSearch for more papers by this author Nathan Seppa, Nathan SeppaSearch for more papers by this author First published: 07 September 2011 https://doi.org/10.1002/scin.5591800621Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume180, Issue610 September 2011Pages 16-16 RelatedInformation

Physical activity, including waking, in relation to cognitive decline in women with cerebrovascular disease or vascular factors

Physical activity, including waking, in relation to cognitive decline in women with cerebrovascular disease or vascular factors

Monounsaturated, trans, and saturated Fatty acids and cognitive decline in women.

To prospectively assess effects of select dietary fats on cognitive decline. Prospective observational; 3-year follow-up. Northwestern University. Four hundred eighty-two women aged 60 and older who participated in the Women's Health Initiative (WHI) Observational Study or in the control group of the WHI Diet Modification arm. Dietary intake from a validated food frequency questionnaire (FFQ) administered twice (mean 2.7 years apart) before baseline cognitive assessment (mean 2.9 years after second FFQ) was averaged. Testing of memory, vision, executive function, language, and attention was performed twice, 3 years apart. A global Z-score was created for both time points by averaging all Z-scores for each participant, and global cognitive change was defined as the difference between follow-up and baseline Z-scores. Median intake of saturated fat (SFA), trans-fat, (TFA), dietary cholesterol (DC), and monounsaturated fat (MUFA) was 18.53, 3.45, 0.201, and 19.39 g/d, respectively. There were no associations between degree of cognitive decline and intake of SFA (P=.69), TFA (P=.54), or DC (P=.64) after adjusting for baseline cognition, total energy intake, age, education, reading ability, apolipoprotein E ɛ4 allele, body mass index, estrogen and beta-blocker use, and intake of caffeine and other fatty acids. In contrast, MUFA intake was associated with lower cognitive decline in fully adjusted linear regression models, with mean decline (standard error) of 0.21 (0.05) in the lowest and 0.05 (0.05) in the highest quartiles (P=.02). This effect of MUFA intake was primarily in the visual and memory domains (P=.03 for both). Greater intake of SFA, TFA, and DC was not associated with cognitive decline, whereas greater MUFA intake was associated with less cognitive decline.

Caffeine Intake is Associated with a Lower Risk of Cognitive Decline: A Cohort Study from Portugal

Alzheimer's disease has emerged in recent decades as a major health problem and the role of lifestyles in the modulation of risk has been increasingly recognized. Recent epidemiological studies suggest a protective effect for caffeine intake in dementia. We aimed to quantify the association between caffeine dietary intake and cognitive decline, in a cohort of adults living in Porto. A cohort of 648 subjects aged > or =65 years was recruited between 1999-2003. Follow-up evaluation (2005-2008) was carried out on 58.2% of the eligible participants and 10.9% were deceased. Caffeine exposure in the year preceding baseline evaluation was assessed with a validated food frequency questionnaire. Cognitive evaluation consisted of baseline and follow-up Mini-Mental State Examination (MMSE). Cognitive decline was defined by a decrease > or =2 points in the MMSE score between evaluations. Relative risk (RR) and 95% confidence interval (95%CI) estimates adjusted for age, education, smoking, alcohol drinking, body mass index, hypertension, and diabetes were computed using Poisson regression. Caffeine intake (> 62 mg/day [3rd third] vs. < 22 mg/day [1st third]) was associated with a lower risk of cognitive decline in women (RR=0.49, 95%CI 0.24-0.97), but not significantly in men (RR=0.65, 95%CI 0.27-1.54). Our study confirms the negative association between caffeine and cognitive decline in women.

The relation between moderate alcohol consumption and cognitive function in older women with type 2 diabetes

Aims To examine the association between moderate drinking, cognitive function, and cognitive decline in women with type 2 diabetes. Methods From 1995 to 2001, we assessed cognitive function in 1698 women aged 71–80 years with type 2 diabetes in the Nurses’ Health Study. Assessments were repeated twice at 2-year intervals. We used linear regression to estimate multivariable-adjusted mean differences in initial cognitive function and longitudinal models to estimate cognitive decline over 4 years, according to average alcohol intake between diagnosis with diabetes and the initial cognitive measurement. Results At the initial assessment, the mean score on our test of general cognition was 0.31 (95% CI 0.02, 0.60) points higher in women who were moderate alcohol drinkers (those consuming 1.0–9.9 g of alcohol, or about 1 drink, per day) compared with abstainers. However, moderate alcohol was not associated with cognitive decline. Higher alcohol consumption (10.0–30.0 g of alcohol per day) was not associated with initial cognition or cognitive decline, although there was no apparent harm either. Conclusions Among women with type 2 diabetes, moderate alcohol was associated with better initial cognition, but not reduced rates of cognitive decline. Thus, we found no clear and consistent cognitive benefits of moderate alcohol in diabetes.

Dietary Fat Intake and Cognitive Decline in Women With Type 2 Diabetes

OBJECTIVEIndividuals with type 2 diabetes have high risk of late-life cognitive impairment, yet little is known about strategies to modify risk. Targeting insulin resistance and vascular complications—both associated with cognitive decline—may be a productive approach. We investigated whether dietary fat, which modulates glucose and lipid metabolism, might influence cognitive decline in older adults with diabetes.RESEARCH DESIGN AND METHODSBeginning in 1995–1999, we evaluated cognitive function in 1,486 Nurses' Health Study participants, aged ≥70 years, with type 2 diabetes; second evaluations were conducted 2 years later. Dietary fat intake was assessed regularly beginning in 1980; we considered average intake from 1980 (at midlife) through initial cognitive interview and also after diabetes diagnosis. We used multivariate-adjusted linear regression models to obtain mean differences in cognitive decline across tertiles of fat intake.RESULTSHigher intakes of saturated and trans fat since midlife, and lower polyunsaturated to saturated fat ratio, were each highly associated with worse cognitive decline in these women. On a global score averaging all six cognitive tests, mean decline among women in the highest trans fat tertile was 0.15 standard units worse than that among women in the lowest tertile (95% CI −0.24 to −0.06, P = 0.002); this mean difference was comparable with the difference we find in women 7 years apart in age. Results were similar when we analyzed diet after diabetes diagnosis.CONCLUSIONSThese findings suggest that lower intakes of saturated and trans fat and higher intake of polyunsaturated fat relative to saturated fat may reduce cognitive decline in individuals with type 2 diabetes.

Women’s cognitive health special edition

Women’s cognitive health special edition

Risk factors for vascular dementia: Hypotension as a key point

Physiologically, the cerebral autoregulation system allows maintenance of constant cerebral blood flow over a wide range of blood pressure. In old people, there is a progressive reshape of cerebral autoregulation from a sigmoid curve to a straight line. This implies that any abrupt change in blood pressure will result in a rapid and significant change in cerebral blood flow. Hypertension has often been observed to be a risk factor for vascular dementia (VaD) and sometimes for Alzheimer disease although not always. Indeed, high blood pressure may accelerate cerebral white matter lesions, but white matter lesions have been found to be facilitated by excessive fall in blood pressure, including orthostatic dysregulation and postprandial hypotension. Many recent studies observed among other data, that there was a correlation between systolic pressure reduction and cognitive decline in women, which was not accounted for by other factors. Baseline blood pressure level was not significantly related to cognitive decline with initial good cognition. Some researchers speculate that blood pressure reduction might be an early change of the dementing process. The most confounding factor is that low pressure by itself might be a predictor of death; nevertheless, the effect of low blood pressure on cognition is underestimated because of a survival bias. Another explanation is that clinically unrecognized vascular lesions in the brain or atherosclerosis are responsible for both cognitive decline and blood pressure reduction. We discuss the entire process, and try to define a possible mechanism that is able to explain the dynamic by which hypotension might be related to dementia.

The Neuroendocrine Effects of Traumatic Brain Injury

The Neuroendocrine Effects of Traumatic Brain Injury

The Neuroendocrine Effects of Traumatic Brain Injury

Neuroendocrine dysfunction after traumatic brain injury (TBI) is under-diagnosed, under-treated, and may adversely affect the rate of recovery. Single or multiple pituitary-target hormone disruption occurs in up to two-thirds of persons with TBI, most commonly affecting the gonadal and growth hormone axes. The time course of decline in and recovery of pituitary function in relation to cognitive dysfunction and rehabilitation progress are not well described. This article reviews the clinical spectrum of neuroendocrine deficits after TBI and their underlying mechanisms. Future studies of the effects of hormonal replacement on recovery are recommended.

The neuroprotective effects of caffeine

To examine the association between caffeine intake, cognitive decline, and incident dementia in a community-based sample of subjects aged 65 years and over. Participants were 4,197 women and 2,820 men from a population-based cohort recruited from three French cities. Cognitive performance, clinical diagnosis of dementia, and caffeine consumption were evaluated at baseline and at 2 and 4 year follow-up. Caffeine consumption is associated with a wide range of sociodemographic, lifestyle, and clinical variables which may also affect cognitive decline. Multivariate mixed models and multivariate adjusted logistic regression indicated that women with high rates of caffeine consumption (over three cups per day) showed less decline in verbal retrieval (OR = 0.67, CI = 0.53, 0.85), and to a lesser extent in visuospatial memory (OR = 0.82, CI = 0.65, 1.03) over 4 years than women consuming one cup or less. The protective effect of caffeine was observed to increase with age (OR = 0.73, CI = 0.53, 1.02 in the age range 65 to 74; OR = 0.3, CI = 0.14, 0.63 in the range 80+). No relation was found between caffeine intake and cognitive decline in men. Caffeine consumption did not reduce dementia risk over 4 years. The psychostimulant properties of caffeine appear to reduce cognitive decline in women without dementia, especially at higher ages. Although no impact is observed on dementia incidence, further studies are required to ascertain whether caffeine may nonetheless be of potential use in prolonging the period of mild cognitive impairment in women prior to a diagnosis of dementia.

Meta-Analyses of the Effect of Hormone Treatment on Cognitive Function in Postmenopausal Women

As we age, most of us experience a certain degree of cognitive decline. In most cases, this decline is gradual. However, in some cases, cognitive impairment is so severe that it can be classified as dementia and this impacts greatly on activities of daily living. Alzheimer's disease, the most common form of dementia, has been linked to the reduction in estrogen levels that comes with aging. More specifically, many researchers have hypothesized that estrogen, and hence estrogen replacement via hormone therapy, could protect against cognitive decline in women. However, recent randomized, controlled trials did not reflect this. In fact, some reports showed that hormone therapy could have detrimental effects on cognitive function in older postmenopausal women. The most publicized of these has been the Women's Health Initiative Memory Study. Studies have thus yielded conflicting results and conclusions. The reasons for this may be due to a number of factors, such as the age of participants, the time of hormone therapy onset ('window of opportunity' theory), type of treatment, type of menopause (surgical or natural) and, possibly, genetic risk factors. We performed quantitative and qualitative meta-analyses and reviewed each of these factors in detail. The future may lie in combining these factors in order to fully understand the potential mechanisms behind estrogen and its effect on cognition.

Homocysteine, estrogen and cognitive decline

Background Factors that contribute to cognitive decline in women from midlife remain poorly understood. There are circumstantial data indicating a positive association between homocysteine and cognitive decline and that endogenous and exogenous estrogen may influence homocysteine levels. The aim of this review was to establish what is known of the relationships between cognitive change and homocysteine levels, and the impact of the menopause transition and exogenous estrogen on homocysteine levels.Methods We reviewed the recent published literature from 1993 to 2005 pertaining to the current understanding of the relationship(s) between plasma homocysteine levels and cognitive functioning and endogenous hormone levels and exogenous estrogen use in women.Results Hyperhomocysteinemia is consistently associated with cognitive decline. Dietary supplementation with vitamins may assist in normalizing homocysteine levels; however, there is no evidence that this results in favorable effects on cognition. Changes in endogenous estrogen levels are inversely associated with changes in serum homocysteine. Consistent with this, estrogen therapy is associated with reductions in plasma homocysteine, with the greatest effects reported in women with higher levels of homocysteine at baseline. Limited data indicate that tibolone is associated with little change in homocysteine. The use of raloxifene, the most studied selective estrogen receptor modulator, is associated with a modest reduction in homocysteine.Conclusions There are data to suggest an underlying link between homocysteine levels and cognitive decline. There is also evidence for a link between both the menopause transition and use of exogenous estrogen therapy and homocysteine levels. Clinical data do not support a role for exogenous estrogen in the prevention of dementia in older women; however, the ‘window of opportunity’ theory suggests that there is a need for randomized controlled trials to evaluate the role of estrogen in the early postmenopausal years to protect against cognitive decline in later life.

Estrogen therapy and risk of cognitive decline: Results from the Women's Estrogen for Stroke Trial (WEST)

This study was undertaken to assess whether estrogen therapy (ET) reduces the risk of cognitive decline in women with cerebrovascular disease. We conducted a randomized, double-blind trial of estradiol 17beta versus placebo for secondary stroke prevention in 664 postmenopausal women with a recent stroke or transient ischemic attack. The Mini-Mental State Examination (MMSE) and 5 domain measures were obtained at baseline and exit. Among 461 women withdrawn alive without stroke, ET did not have a significant effect on cognitive measures after an average of 3 years (relative risk of MMSE decline: 0.74, 95% CI, 0.49-1.13). In women with normal MMSE at entry, estrogen was associated with less decline (relative risk, 0.46, 95% CI, 0.24-0.87). In this study, estradiol did not have significant effects on cognitive measures. However, in women with normal function at baseline, there may be a benefit for ET in reducing the risk for cognitive decline.

P2-283 Fruit and vegetable consumption and cognitive decline in women

P2-283 Fruit and vegetable consumption and cognitive decline in women