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Cognitive decline

About: Cognitive decline is a research topic. Over the lifetime, 29308 publications have been published within this topic receiving 1174689 citations.


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TL;DR: Hearing loss is independently associated with lower scores on the Digit Symbol Substitution Test, and whether hearing loss is a modifiable risk factor or an early marker of cognitive decline is needed.
Abstract: sample of older adults. Methods. We analyzed data from the 1999 to 2002 cycles of the National Health and Nutritional Examination Survey during which participants aged 60–69 years (n = 605) underwent both audiometric and cognitive testing. Hearing loss was defined by a pure tone average of hearing thresholds at 0.5, 1, 2, and 4 kHz in the better hearing ear. Cognitive testing consisted of the Digit Symbol Substitution Test (DSST), a nonverbal test that assesses executive function and psychomotor processing. Data on hearing aid use, demographics, and medical history were obtained from interviews. Regression models were used to examine the association between hearing loss and cognition while adjusting for confounders. Analyses incorporated sampling weights to yield results that are generalizable to the U.S. population. Results. Greater hearing loss was significantly associated with lower scores on the DSST after adjustment for demo graphic factors and medical history (DSST score difference of −1.5 [95% confidence interval : −2.9 to −0.23] per 10 dB of hearing loss). Hearing aid use was positively associated with cognitive functioning (DSST score difference of 7.4 [95% confidence interval : −0.62 to 15.4]). The reduction in cognitive performance associated with a 25 dB hearing loss was equivalent to the reduction associated with an age difference of 7 years. Conclusions. Hearing loss is independently associated with lower scores on the DSST. Further research is needed to determine whether hearing loss is a modifiable risk factor or an early marker of cognitive decline.

428 citations

Journal ArticleDOI
TL;DR: The results show that B-vitamin supplementation can slow the atrophy of specific brain regions that are a key component of the AD process and that are associated with cognitive decline, and further trials focusing on elderly subjets with high homocysteine levels are warranted.
Abstract: Is it possible to prevent atrophy of key brain regions related to cognitive decline and Alzheimer’s disease (AD)? One approach is to modify nongenetic risk factors, for instance by lowering elevated plasma homocysteine using B vitamins. In an initial, randomized controlled study on elderly subjects with increased dementia risk (mild cognitive impairment according to 2004 Petersen criteria), we showed that high-dose B-vitamin treatment (folic acid 0.8 mg, vitamin B6 20 mg, vitamin B12 0.5 mg) slowed shrinkage of the whole brain volume over 2 y. Here, we go further by demonstrating that B-vitamin treatment reduces, by as much as seven fold, the cerebral atrophy in those gray matter (GM) regions specifically vulnerable to the AD process, including the medial temporal lobe. In the placebo group, higher homocysteine levels at baseline are associated with faster GM atrophy, but this deleterious effect is largely prevented by B-vitamin treatment. We additionally show that the beneficial effect of B vitamins is confined to participants with high homocysteine (above the median, 11 µmol/L) and that, in these participants, a causal Bayesian network analysis indicates the following chain of events: B vitamins lower homocysteine, which directly leads to a decrease in GM atrophy, thereby slowing cognitive decline. Our results show that B-vitamin supplementation can slow the atrophy of specific brain regions that are a key component of the AD process and that are associated with cognitive decline. Further B-vitamin supplementation trials focusing on elderly subjets with high homocysteine levels are warranted to see if progression to dementia can be prevented.

427 citations

Journal ArticleDOI
TL;DR: The main hypothesis was that subtle vitamin B12 deficiencies occur more commonly in senile dementia of Alzheimer type (SDAT) than in healthy elderly individuals, and may be revealed by elevated total serum homocysteine (tHcy).
Abstract: Objective. The main hypothesis was that subtle vitamin B12 deficiencies occur more commonly in senile dementia of Alzheimer type (SDAT) than in healthy elderly individuals, and may be revealed by elevated total serum homocysteine (tHcy). A subsidiary hypothesis was that such deficiencies would be nutritionally independent as determined by retinol binding protein (RBP). Design. A prospective case-controlled survey. Setting. A Welsh urban psychogeriatric assessment centre and local general practice. Patients. Thirty patients, aged 65 or over, seen consecutively in 1994 with features compatible with DSM-III-R criteria for primary degenerative dementia of Alzheimer type and 30 cognitively intact age-matched control subjects. Measures. Diagnosis was assessed using the CAMDEX. Cognitive scores were evaluated with the CAMCOG scale for patients and MMSE scores for control subjects. tHcy was measured using high performance liquid chromatography (HPLC), and RBP assayed by a radial immunodiffusion method. Results. Patients had a highly significant elevation of tHcy compared with controls (p<0·0001). Multiple regression highlighted the interrelated effects of tHcy and total serum cobalamin on cognitive scores. RBP did not differ between groups. Macrocytosis was absent, and neutrophil hypersegmentation uncommon, in hyperhomocysteinaemic patients. Conclusions. SDAT patients have significantly elevated tHcy. This is independent of RBP determined nutritional status. ‘Classical’ haematological changes of cobalamin or folate deficiency are poor predictors of tHcy in these patients. Aberrant cobalamin tissue delivery appears to contribute to SDAT cognitive decline. Relative contributions of other tHcy determinants require further investigation. © 1998 John Wiley & Sons, Ltd.

427 citations

Journal ArticleDOI
TL;DR: It is found, in two separate human studies, that 1/f electrophysiological noise increases with aging, and it is observed that this age-related 1/ f noise statistically mediates age- related working memory decline.
Abstract: Aging is associated with performance decrements across multiple cognitive domains. The neural noise hypothesis, a dominant view of the basis of this decline, posits that aging is accompanied by an increase in spontaneous, noisy baseline neural activity. Here we analyze data from two different groups of human subjects: intracranial electrocorticography from 15 participants over a 38 year age range (15-53 years) and scalp EEG data from healthy younger (20-30 years) and older (60-70 years) adults to test the neural noise hypothesis from a 1/f noise perspective. Many natural phenomena, including electrophysiology, are characterized by 1/f noise. The defining characteristic of 1/f is that the power of the signal frequency content decreases rapidly as a function of the frequency (f) itself. The slope of this decay, the noise exponent (χ), is often <-1 for electrophysiological data and has been shown to approach white noise (defined as χ = 0) with increasing task difficulty. We observed, in both electrophysiological datasets, that aging is associated with a flatter (more noisy) 1/f power spectral density, even at rest, and that visual cortical 1/f noise statistically mediates age-related impairments in visual working memory. These results provide electrophysiological support for the neural noise hypothesis of aging. Significance statement: Understanding the neurobiological origins of age-related cognitive decline is of critical scientific, medical, and public health importance, especially considering the rapid aging of the world's population. We find, in two separate human studies, that 1/f electrophysiological noise increases with aging. In addition, we observe that this age-related 1/f noise statistically mediates age-related working memory decline. These results significantly add to this understanding and contextualize a long-standing problem in cognition by encapsulating age-related cognitive decline within a neurocomputational model of 1/f noise-induced deficits in neural communication.

424 citations

Journal ArticleDOI
TL;DR: It is raised the possibility that dietary flavonoid intake is associated with better cognitive evolution, as well as several other potential confounders, after adjustment for age, sex, and educational level.
Abstract: In the PAQUID (Personnes Agees Quid) study, the authors prospectively examined flavonoid intake in relation to cognitive function and decline among subjects aged 65 years or older. A total of 1,640 subjects free from dementia at baseline in 1990 and with reliable dietary assessment were reexamined four times over a 10-year period. Cognitive functioning was assessed through three psychometric tests (Mini-Mental State Examination, Benton's Visual Retention Test, "Isaacs" Set Test) at each visit. Information on flavonoid intake was collected at baseline. A linear mixed model was used to analyze the evolution of cognitive performance according to quartiles of flavonoid intake. After adjustment for age, sex, and educational level, flavonoid intake was associated with better cognitive performance at baseline (p = 0.019) and with a better evolution of the performance over time (p = 0.046). Subjects included in the two highest quartiles of flavonoid intake had better cognitive evolution than did subjects in the lowest quartile. After 10 years' follow-up, subjects with the lowest flavonoid intake had lost on average 2.1 points on the Mini-Mental State Examination, whereas subjects with the highest quartile had lost 1.2 points. This gradient persisted after adjustment for several other potential confounders. This study raises the possibility that dietary flavonoid intake is associated with better cognitive evolution.

423 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023914
20221,895
20213,389
20202,982
20192,551
20182,022