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PubMed2001

Evidence for cortical "disconnection" as a mechanism of age-related cognitive decline.

BACKGROUND: Normal aging is accompanied by a decline of cognitive abilities, and executive skills may be affected selectively, but the underlying mechanisms remain obscure and preventive strategies are lacking. It has been suggested that cortical "disconnection" due to the loss of white matter fibers may play an important role. But, to date, there has been no direct demonstration of structural disconnection in humans in vivo. METHODS: The authors used diffusion tensor MRI to look for evidence of ultrastructural changes in cerebral white matter in a group of 20 elderly volunteers with normal conventional MRI scans, and a group of 10 younger controls. The older group also underwent neuropsychological assessment. RESULTS: Diffusional anisotropy, a marker of white matter tract integrity, was reduced in the white matter of older subjects and fell linearly with increasing age in the older group. Mean diffusivity was higher in the older group and increased with age. These changes were maximal in anterior white matter. In the older group, anterior mean diffusivity correlated with executive function assessed by the Trail Making Test. CONCLUSIONS: These findings provide direct evidence that white matter tract disruption occurs in normal aging and would be consistent with the cortical disconnection hypothesis of age-related cognitive decline. Maximal changes in anterior white matter provide a plausible structural basis for selective loss of executive functions. In addition to providing new information about the biological basis of cognitive abilities, diffusion tensor MRI may be a sensitive tool for assessing interventions aimed at preventing cognitive decline.

Adult↗

PubMed2006

PET network abnormalities and cognitive decline in patients with mild cognitive impairment.

Temporoparietal and posterior cingulate metabolism deficits characterize patients with Alzheimer's disease (AD). A H(2)(15)O resting PET scan covariance pattern, derived by using multivariate techniques, was previously shown to discriminate 17 mild AD patients from 16 healthy controls. This AD covariance pattern revealed hypoperfusion in bilateral inferior parietal lobule and cingulate; and left middle frontal, inferior frontal, precentral, and supramarginal gyri. The AD pattern also revealed hyperperfusion in bilateral insula, lingual gyri, and cuneus; left fusiform and superior occipital gyri; and right parahippocampal gyrus and pulvinar. In an independent sample of 23 outpatients with mild cognitive impairment (MCI) followed at 6-month intervals, the AD pattern score was evaluated as a predictor of cognitive decline. In this MCI sample, an H2(15)O resting PET scan was carried out at baseline. Mean duration of follow-up was 48.8 (SD 15.5) months, during which time six of 23 MCI patients converted to AD. In generalized estimating equations (GEE) analyses, controlling for age, sex, education, and baseline neuropsychological scores, increased AD pattern score was associated with greater decline in each neuropsychological test score over time (Mini Mental State Exam, Selective Reminding Test delayed recall, Animal Naming, WAIS-R digit symbol; Ps<0.01-0.001). In summary, a resting PET covariance pattern previously reported to discriminate AD patients from control subjects was applied prospectively to an independent sample of MCI patients and found to predict cognitive decline. Independent replication in larger samples is needed before clinical application can be considered.

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PubMed2006

Changes in Mini Mental State Examination score after stroke: lacunar infarction predicts cognitive decline.

Stroke and cognitive impairment are inter-related. The purpose of this study was to show the natural evolution of cognitive performance during the first year after a stroke, and to show which factors that predict cognitive decline. Subjects were patients with a first-ever stroke who were treated in a stroke unit. A total of 160 patients were included. At baseline patients were evaluated with regard to stroke type, stroke severity, pre-stroke dementia and other risk factors. Mini Mental State Examinations (MMSE) were performed after 1 week and after 1 year. Patients had a median increase of 1 point (range -8 to +9) on the MMSE. Thirty-two pre cent of the patients deteriorated, 13% were unchanged, and 55% improved. Lacunar infarction (LI) and left-sided stroke were associated with a failure to exhibit improvement. Patients with LI had an average decline of 1.7 points, whilst patients with other stroke types had an average increase of 1.8 points. Most stroke survivors improve cognitively during the first year after the event. The outcome for LI patients is worse, which suggests that LI may serve as a marker for concomitant processes that cause cognitive decline.

Analysis of Variance↗

PubMedDate not supplied

Correlates of informant-rated cognitive decline after stroke.

Cognitive impairment is common after stroke, but measurement is problematic. Six tests of mental ability, unaffected by loss of limb function, were administered to 49 subjects of mean age 74.2 years at a median of 4.3 years (range 0.1-16.8) after stroke together with a depression score and the IQCODE, an informant-rated scale of estimated cognitive decline. Over 90% of stroke patients were able to complete most tests. IQCODE correlated significantly with the HADS depression score (r = 0.35, p = 0.040), the 2-year Barthel score (r = -0.60, p = 0.001) and with a general cognitive factor extracted from the mental ability test scores (r = -0.42, p = 0.016). We conclude that informant-rated methods offer a promising approach to measuring cognitive decline after stroke.

Activities of Daily Living↗

PubMed1996

Informant ratings of cognitive decline of elderly people: relationship to longitudinal change on cognitive tests.

Formal assessment of cognitive decline with cognitive tests can be difficult, requiring either two measurement points or a comparison of 'hold' with 'don't hold' tests. Informant-based assessment provides an alternative approach because informants can adopt a longitudinal perspective and directly rate cognitive change. A study was carried out to assess the validity of informant ratings collected by means of the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE). A community sample of 500 subjects aged 74 or over underwent four cognitive tests on two occasions 3 1/2 years apart. On the second occasion, informants filled out the IQCODE. Subjects rated as having moderate or severe decline were found to have greater change on the cognitive tests. These findings support the validity of informant ratings of cognitive decline.

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PubMed1996

Informant ratings of cognitive decline of elderly people: relationship to longitudinal change on cognitive tests

Formal assessment of cognitive decline with cognitive tests can be difficult, requiring either two measurement points or a comparison of 'hold' with 'don't hold' tests. Informant-based assessment provides an alternative approach because informants can adopt a longitudinal perspective and directly rate cognitive change. A study was carried out to assess the validity of informant ratings collected by means of the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE). A community sample of 500 subjects aged 74 or over underwent four cognitive tests on two occasions 3&half; years apart. On the second occasion, informants filled out the IQCODE. Subjects rated as having moderate or severe decline were found to have greater change on the cognitive tests. These findings support the validity of informant ratings of cognitive decline.

Journal Article↗

PubMed2006

Demonstration of cognitive decline in Parkinson's disease using the Cambridge Cognitive Assessment (Revised) (CAMCOG-R).

BACKGROUND: Cognitive impairment is well recognised in Parkinson's Disease (PD) but few studies have examined cognitive decline over time in such subjects. Standard clinical assessments of cognitive function, such as the MMSE, do not measure all cognitive domains and often have a ceiling effect. CAMCOG-R provides a more comprehensive cognitive assessment allowing several different domains of cognition to be compared. It also features the ability to test 'executive function'. CAMCOG-R has only been reported on one previous occasion in PD subjects and this is the first study to report a follow-up CAMCOG-R to assess cognitive decline. METHODS: In a previously published study CAMCOG-R was administered to a prevalent community-based population of 94 subjects with PD with a MMSE of 25 or above. In this subsequent study 85 of the subjects (two declined and seven were deceased) underwent a follow-up CAMCOG-R after a mean delay of 13.1 months. RESULTS: The initial, and follow-up mean total CAMCOG-R scores were 88.65/104 and 84.75/104 respectively, demonstrating a significant decline (p < 0.05). Significant cognitive decline (p < 0.05) was also seen across every CAMCOG-R cognitive domain and in the executive function scores. CONCLUSIONS: A wide range of cognitive ability was again demonstrated using CAMCOG-R in this PD population. The decline of 3.9 CAMCOG-R points over the 13-month period compares to other previous studies showing an annual decline of 1.6 CAMCOG points in normal elderly individuals and 12 CAMCOG points annually in those with established dementia. This study suggests that CAMCOG-R is a useful and appropriate tool for use in follow-up cognitive screening in PD subjects.

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PubMed2000

Informant ratings of cognitive decline in old age: validation against change on cognitive tests over 7 to 8 years.

BACKGROUND: Informant questionnaires on cognitive decline are increasingly used as screening tests for dementia. Informants can provide a longitudinal perspective that is not possible with cognitive screening tests administered at one point in time. However, there are limited data on the validity of such questionnaires when judged against longitudinal change on cognitive tests. METHODS: A community sample of elderly people aged > or = 70 was assessed on cognitive tests at baseline and after a follow-up of 7-8 years. The participants were given the Mini-Mental State Examination and tests of episodic memory and mental speed. At follow-up, the short-form of the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE) was completed by informants for 287 of the participants. RESULTS: Elderly people who were rated by informants as having moderate or severe decline had declined significantly on cognitive tests. The IQCODE correlated as highly with cognitive test change scores as these change scores correlated with each other. CONCLUSIONS: The IQCODE is a valid way of assessing cognitive decline when assessment can be carried out only at one point in time.

Age Factors↗

PubMed1998

Blood pressure reduction, cardiovascular diseases, and cognitive decline in the mini-mental state examination in a community population of normal very old people: a three-year follow-up.

We observed the decline in cognitive functioning in a community cohort of 924 persons aged > or =75 years with initially good cognition. Cognitive performance was indexed with the Mini-Mental State Examination (MMSE) on two occasions, 3 years apart. The average decline in MMSE score was 0.4 points per year. However, 23.4% of the participants lost more than 10% of their baseline MMSE scores. Women declined more rapidly than men. Baseline advanced age, lower education, and stroke predicted the greater decline in women. It appears that the relation of lower education and stroke with cognitive decline was more pronounced in men, but age did not predict cognitive decline in men. In addition, there was a correlation between systolic pressure reduction and cognitive decline in women, which was not accounted for by other factors. In summary, although the cognitive ability is generally spared longitudinally, in terms of the entire population, a considerable proportion of individuals show substantial decline that is related to several factors such as advanced age, female gender, lower education, stroke, and systolic pressure reduction.

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PubMed2006

Translational gene mapping of cognitive decline.

The ability to maintain cognitive function during aging is a complex process subject to genetic and environmental influences. Alzheimer's disease (AD) is the most common disorder causing cognitive decline among the elderly. Among those with AD, there is broad variation in the relationship between AD neuropathology and clinical manifestations of dementia. Differences in expression of genes involved in neural processing pathways may contribute to individual differences in maintenance of cognitive function. We performed whole genome expression profiling of RNA obtained from frontal cortex of clinically non-demented and AD subjects to identify genes associated with brain aging and cognitive decline. Genetic mapping information and biological function annotation were incorporated to highlight genes of particular interest. The candidate genes identified in this study were compared with those from two other studies in different tissues to identify common underlying transcriptional profiles. In addition to confirming sweeping transcriptomal differences documented in previous studies of cognitive decline, we present new evidence for up-regulation of actin-related processes and down-regulation of translation, RNA processing and localization, and vesicle-mediated transport in individuals with cognitive decline.

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PubMed2005

Age-related neuropathology, cognitive decline, and Alzheimer's disease.

In the last 20 years, there have been tremendous strides made in the understanding of the molecular and cellular processes that occur during brain aging, as well as our understanding of age-related disorders of the central nervous system (CNS). Aging is associated with a decline in cognitive performance, and is the biggest risk factor for the development of Alzheimer's disease (AD), although the underlying basis for both of these observations is poorly defined. Both normal aging and AD are associated with overlapping and increased levels of pathology. Numerous reports have now linked elevations in pathology as potential mediators of cognitive decline in the elderly, with most studies focusing on the role of AD-related pathology. However, it is important to point out that there are numerous other pathological features observed in the aging brain including corpora amylacea, argyrophilic grains, neuromelanin, and lipofuscin. In this review, I discuss the decreased cognitive performance observed during normal aging, the potential for pathology to alter neuronal function and neuronal viability during normal brain aging, and the potential for common pathologies to either inhibit or promote the development of age-related disorders such as AD.

Aging↗

PubMed2006

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.

Cognition↗

PubMed2006

Endogenous sex hormones, cognitive decline, and future dementia in old men.

OBJECTIVE: To estimate the association of endogenous levels of bioavailable testosterone and estradiol with risk for cognitive decline and dementia in old men. METHODS: Within the population-based, prospective Honolulu-Asia Aging Study, 2,974 men, aged 71 to 93 years, without dementia were reexamined 3 times over an average of 6 years for development of dementia and cognitive decline. Cognitive decline was measured with the Cognitive Abilities Screening Instrument. Incident dementia was diagnosed according to standard criteria. A total of 134 men experienced development of Alzheimer's disease (AD; including 40 cases with contributing cerebrovascular disease) and 44 experienced development of vascular dementia. RESULTS: Adjusting for age and other covariates, testosterone was not associated with risk for dementia (using Cox regression analyses) or cognitive decline (using random coefficient analyses). However, higher levels of estradiol were associated with risk for AD (hazard ratio per standard deviation increase, 1.25; 95% confidence interval, 1.05-1.47) and AD with cerebrovascular disease (hazard ratio, 1.19; 95% confidence interval, 1.02-1.38). Also, compared with the lowest tertile of estradiol, men in the middle and highest tertile of estradiol had 0.24 and 0.28 points lower Cognitive Abilities Screening Instrument scores, respectively, for each year increase in age. INTERPRETATION: In old men, endogenous testosterone levels are not associated with risk for cognitive decline and AD, whereas higher estrogen levels increase risk for cognitive decline and AD.

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PubMed2006

Handgrip strength and cognitive decline in older Mexican Americans.

BACKGROUND: Cognitive decline and dementia are associated with disability and premature death in old age. We examined whether low handgrip strength predicts subsequent cognitive decline in older Mexican Americans. METHODS: We worked with a 7-year prospective cohort of 2160 noninstitutionalized Mexican Americans aged 65 years or older from the Hispanic Established Population for the Epidemiological Study of the Elderly (H-EPESE) who had a Mini-Mental State Examination (MMSE) score > or = 21 at baseline. Measures included: (i) sociodemographic factors (age, gender, and education), handgrip strength, and near and distant visual impairment from baseline interview; and (ii) MMSE, body mass index (BMI), and medical conditions (stroke, heart attack, diabetes, depression, and hypertension) from four waves of data collection. RESULTS: Using general linear mixed models, we found a significant trend with scores in the lowest quartile of handgrip strength at baseline to be associated with lower MMSE scores over time (estimate = -1.28, standard error = 0.16; p <.0001). There was a significant handgrip Strength-by-Time interaction with MMSE scores. Participants in the lowest handgrip strength quartile had a greater cognitive decline over time (estimate = -0.26, standard error = 0.07; p <.001) than did those participants in the highest quartile. This association remained statistically significant after controlling for potential confounding factors. CONCLUSION: Older Mexican Americans with reduced handgrip strength at baseline demonstrated a statistically significant decline in cognitive function over a 7-year period. By contrast, participants in the highest handgrip strength quartile maintained a higher level of cognitive function.

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PubMed2003

The role of diet in cognitive decline.

Recent findings suggest a possible role of diet in age-related cognitive decline, and cognitive impairment of both degenerative (Alzheimer's disease, AD) or vascular origin. In particular, in an older population of Southern Italy with a typical Mediterranean diet, high monounsaturated fatty acids energy intake appeared to be associated with a high protection against cognitive decline. In addition, dietary fat and energy in older people seem to be risk factors, while fish consumption and cereals are found to reduce the prevalence of AD in the European and North American countries. Moreover, foods with large amounts of aluminium-containing additives or aluminium from drinking water may affect the risk of developing AD. Vitamin deficiencies, especially vitamin B6, B12 and folates, and antioxidant deficiencies (vitamins E and C) could also influence the memory capabilities and have an effect on cognitive decline. Dietary anti-oxidants and supplements and specific macronutrients of the diet may act synergistically with other protective factors opening new possibilities of intervention for cognitive decline.

Aging↗

PubMed2003

Natural history of cognitive decline in the old old.

OBJECTIVE: To prospectively examine the occurrence and outcome of cognitive decline in healthy, community-dwelling elders. METHODS: Ninety-five elders (mean age 84 years) who at entry had no cognitive impairment were followed for up to 13 years. Cognitive decline was defined as obtaining either a Clinical Dementia Rating (CDR) = 0.5 or Mini-Mental State Examination (MMSE) score < 24 on two examinations. RESULTS: Three outcomes of aging were determined: intact cognition, persistent cognitive decline without progression to dementia, and dementia. Whereas 49% remained cognitively intact, 51% developed cognitive decline. Mean follow-up to first CDR 0.5 was 3.8 years and age at conversion was 90.0 years. Those who remained cognitively intact had better memory at entry and were less likely to have APOE4 than those who developed cognitive decline. Of the 48 participants with cognitive decline, 27 (56%) developed dementia (CDR > or =1) a mean of 2.8 years later. Participants with cognitive decline who progressed to dementia had poorer confrontation naming at the time of their first CDR 0.5 than those with persistent cognitive decline who did not progress during follow-up. CONCLUSION: The old old are at high risk for developing cognitive decline but many will not progress to dementia in the next 2 to 3 years or even beyond. These findings are important for understanding the prognosis of cognitive decline and for the design of treatment trials for AD. APOE genotype is a risk factor for cognitive decline.

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PubMed1992

Preventing cognitive decline.

Many studies of age-related cognitive decline have failed to distinguish between usual and successful aging. Although some degree of cognitive impairment is associated with aging, when one looks at average performance, there is great variability among individuals, with many showing little or no deleterious effects of aging on intellectual abilities. Many of the risk factors for dementia and for conditions associated with cognitive impairments can be treated or controlled. Among the preventable causes of cognitive decline are the following: AIDS, Alcohol and drug abuse, Cerebrovascular disease, Exposure to organic solvents or lead, Head trauma, Overmedication, Syphilis. Other conditions that may cause cognitive decline can be controlled or treated: Atherosclerosis, Depression, Diabetes, Emphysema, High blood pressure, Obesity, Sleep disorders, Thyroid dysfunction. In addition, it may be possible to enhance the cognitive performance of even healthy elderly people through changes in diet and lifestyle. Recent data raise the possibility that improved prenatal and perinatal care and greater access to educational opportunities may result in a decreased incidence of dementia in future generations of older adults. Although they are rapidly becoming more numerous, the efficacy of cognitive training programs in preventing or slowing cognitive decline has not yet been demonstrated. Nevertheless, such programs may ameliorate cognitive impairment by reducing the psychiatric disabilities associated with anxiety and depression. The general principle underlying these strategies for limiting cognitive impairment with age is to maximize brain reserve and minimize brain damage.

Aging↗

PubMed1997

Blood pressure and cognitive decline in healthy old people.

Both hypertension and cognitive decline are common in old age. We sought to examine the effects of blood pressure (BP) on rates of cognitive decline in a longitudinal study of community-resident healthy old people. A total of 603 initially healthy old people aged over 69 years were visited at home. Subject's age, years of full-time education, Social Occupational Classification, health status and medication use were recorded. Sitting systolic and diastolic BP was measured, and the Mini-Mental State Examination (MMSE) and National Adult Reading Test (NART) administered. Follow-up was planned after 4 years: 69 subjects were dead, 15 were too unwell and 12 had moved away; 78 subjects either refused or failed to reply. Psychometric tests were administered to the remaining 429 (71.1%) after a median period of 4.20 years. Forty-two subjects had significant sensory impairment or interrupted testing. No significant differences in cognitive decline were found between those who had started medication (n = 163) and those remaining untreated (n = 224). Mean MMSE score change was 0.44 points (s.d. 2.07, P < 0.001). Entering all baseline variables into a stepwise regression analysis significant positive effects were found for initial MMSE score (beta = 0.50, P < 0.001), age (beta = 0.17, P < 0.001), systolic BP (beta = 0.16, P < 0.001) and period between testing (beta = 0.14, P = 0.004), and negative effect for NART-predicted IQ (beta = -0.16, P = 0.003).). We conclude that (1) older people exhibit faster age-associated cognitive decline as measured by MMSE; (2) people with higher NART-predicted IQs are relatively protected; (3) people with high systolic BPs are at greater risk of cognitive decline.

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