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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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Journal ArticleDOI
TL;DR: There is evidence that cognitive speed and memory performance decline with age, but that crystallized abilities remain largely intact in those who survive for long-term follow-up, and education, good health, absence of the APOE ∊4 allele, and activity may be protective of cognitive decline.
Abstract: Background: This paper briefly summarizes recent evidence on the nature of cognitive decline, the variability in individual responses to ageing, and risk factors known to affect the rate of cogniti...

326 citations

Journal ArticleDOI
TL;DR: It is concluded that subjective memory complaints may predict dementia within 3 years, particularly when there are objective signs of memory deterioration.
Abstract: Whether subjective memory complaints in the absence of objective memory decline can predict future dementia has been investigated only in highly selected clinical and volunteer cohorts. Our study examines this question in a subsample of AMSTEL (Amsterdam Study of the Elderly), a longitudinal population study on cognitive decline and dementia. Subjects (aged 65 to 84 years; n = 357) without dementia or other psychiatric disorders at baseline were followed for 3 years. After this interval, 16 of 203 re-examined patients developed a dementia. Logistic regression analyses indicated that memory complaints at baseline contributed a small but significant amount of diagnostic information. However, the most powerful predictor of future dementia was deficient memory performance. We conclude that subjective memory complaints may predict dementia within 3 years, particularly when there are objective signs of memory deterioration.

325 citations

Journal Article
TL;DR: Meta-analyses confirm benefits in major depressive disorder (MDD) and bipolar disorder, with promising results in schizophrenia and initial benefit for borderline personality disorder, and omega-3 phospholipid supplements that combine DHA/EPA andospholipids into the same molecule have shown marked promise in early clinical trials.
Abstract: The omega-3 fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) are orthomolecular, conditionally essential nutrients that enhance quality of life and lower the risk of premature death. They function exclusively via cell membranes, in which they are anchored by phospholipid molecules. DHA is proven essential to pre- and postnatal brain development, whereas EPA seems more influential on behavior and mood. Both DHA and EPA generate neuroprotective metabolites. In double-blind, randomized, controlled trials, DHA and EPA combinations have been shown to benefit attention deficit/hyperactivity disorder (AD/HD), autism, dyspraxia, dyslexia, and aggression. For the affective disorders, meta-analyses confirm benefits in major depressive disorder (MDD) and bipolar disorder, with promising results in schizophrenia and initial benefit for borderline personality disorder. Accelerated cognitive decline and mild cognitive impairment (MCI) correlate with lowered tissue levels of DHA/EPA, and supplementation has improved cognitive function. Huntington disease has responded to EPA. Omega-3 phospholipid supplements that combine DHA/EPA and phospholipids into the same molecule have shown marked promise in early clinical trials. Phosphatidylserine with DHA/EPA attached (Omega-3 PS) has been shown to alleviate AD/HD symptoms. Krill omega-3 phospholipids, containing mostly phosphatidylcholine (PC) with DHA/EPA attached, markedly outperformed conventional fish oil DHA/EPA triglycerides in double-blind trials for premenstrual syndrome/dysmenorrhea and for normalizing blood lipid profiles. Krill omega-3 phospholipids demonstrated anti-inflammatory activity, lowering C-reactive protein (CRP) levels in a double-blind trial. Utilizing DHA and EPA together with phospholipids and membrane antioxidants to achieve a triple cell membrane synergy may further diversify their currently wide range of clinical applications.

325 citations

Journal ArticleDOI
TL;DR: It is concluded that higher education AD patients experience faster cognitive decline, which was present over and above age, gender, ethnicity, differential baseline cognitive performance, depression, and vascular comorbidity.
Abstract: Background: Some (but not all) epidemiological studies have noted faster rates of progression in high education patients with Alzheimer’s disease (AD), which has been attributed to harbouring/tolerating a higher pathological burden at the time of clinical dementia for subjects with higher education. We wanted to assess the relationship between education and rates of decline in AD. Methods: During the course of a community based multiethnic prospective cohort study of individuals aged ⩾65 years living in New York, 312 patients were diagnosed with incident AD and were followed overall for 5.6 (up to 13.3) years. The subjects received an average of 3.7 (up to 9) neuropsychological assessments consisting of 12 individual tests. With the aid of a normative sample, a standardised composite cognitive score as well as individual cognitive domain scores were calculated. Generalised estimating equation models were used to examine the association between education and rates of cognitive decline. Results: Composite cognitive performance declined by 9% of a standard deviation per year. Rates of decline before and after AD incidence were similar. For each additional year of education there was 0.3% standard deviation lower composite cognitive performance for each year of follow up. The association between higher education and faster decline was noted primarily in the executive speed (0.6%) and memory (0.5%) cognitive domains and was present over and above age, gender, ethnicity, differential baseline cognitive performance, depression, and vascular comorbidity. Conclusions: We conclude that higher education AD patients experience faster cognitive decline.

324 citations

Journal ArticleDOI
TL;DR: Higher than expected rates of subclinical epileptiform activity in AD with deleterious effects on cognition are hypothesized, motivated by results from animal studies.
Abstract: OBJECTIVE Seizures are more frequent in patients with Alzheimer's disease (AD) and can hasten cognitive decline. However, the incidence of subclinical epileptiform activity in AD and its consequences are unknown. Motivated by results from animal studies, we hypothesized higher than expected rates of subclinical epileptiform activity in AD with deleterious effects on cognition. METHODS We prospectively enrolled 33 patients (mean age 62 years) who met criteria for AD, but had no history of seizures, and 19 age-matched, cognitively normal controls. Subclinical epileptiform activity was assessed, blinded to diagnosis, by overnight long-term video-electroencephalography and a one-hour resting magnetoencephalography exam with simultaneous EEG. Patients also had comprehensive clinical and cognitive evaluations, assessed longitudinally over an average period of 3.3 years. RESULTS Subclinical epileptiform activity was detected in 42.4% of AD patients and 10.5% of controls (p = 0.02). At the time of monitoring, AD patients with epileptiform activity did not differ clinically from those without such activity. However, patients with subclinical epileptiform activity showed faster declines in global cognition, determined by the Mini-Mental State Examination (3.9 points/year in patients with epileptiform activity vs. 1.6 points/year in patients without, p = 0.006), and in executive function (p = 0.01). INTERPRETATION Extended monitoring detects subclinical epileptiform activity in a substantial proportion of patients with AD. Patients with this indicator of network hyperexcitability are at risk for accelerated cognitive decline and might benefit from antiepileptic therapies. These data call for more sensitive and comprehensive neurophysiological assessments in AD patient evaluations and impending clinical trials. This article is protected by copyright. All rights reserved.

324 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