Cognitive decline

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

Alpha-synuclein-immunoreactive cortical Lewy bodies are associated with cognitive impairment in Parkinson's disease

Abstract: Amygdala, hippocampus and six cortical gyri were examined for the Lewy body (LB) degeneration and Alzheimer’s disease (AD) type changes in 45 patients with Parkinson’s disease (PD). For detection of LBs, the brain areas were stained with an antibody against alpha-synuclein. The extent of neuropathological lesions was investigated in relation to cognitive dysfunction and apolipoprotein E (apoE) ɛ4 allele dosage. At least one cortical LB was found in 95% of cases (43/45). Furthermore, 40% of cases (18/45) had histological findings of definite AD (CERAD class C). Those PD cases with the apoE ɛ4 allele had a significantly greater number of cortical LBs than those without the apoE ɛ4 allele, but this was statistically significant only in precentral, angular and temporal gyri. The LB density correlated better with the number of plaques than with the density of tangles. The number of LBs in several cortical areas correlated significantly with the cognitive impairment. In stepwise linear regression analysis, the number of LBs in the cingulate gyrus and the amount of tangles in the temporal cortex remained statistically significant. When the CERAD class C was excluded, the correlation between cognitive decline and the number of LBs in cortical areas became even more pronounced. A stepwise linear regression analysis in these cases found the number of LBs in the frontal gyrus to be the statistically most significant predictor of cognitive impairment. This study shows, for the first time, that in PD, alpha-synuclein-positive cortical LBs are associated with cognitive impairment independent of AD-type pathology.

The retina in Parkinson's disease

Abstract: As a more complete picture of the clinical phenotype of Parkinson's disease emerges, non-motor symptoms have become increasingly studied. Prominent among these non-motor phenomena are mood disturbance, cognitive decline and dementia, sleep disorders, hyposmia and autonomic failure. In addition, visual symptoms are common, ranging from complaints of dry eyes and reading difficulties, through to perceptual disturbances (feelings of presence and passage) and complex visual hallucinations. Such visual symptoms are a considerable cause of morbidity in Parkinson's disease and, with respect to visual hallucinations, are an important predictor of cognitive decline as well as institutional care and mortality. Evidence exists of visual dysfunction at several levels of the visual pathway in Parkinson's disease. This includes psychophysical, electrophysiological and morphological evidence of disruption of retinal structure and function, in addition to disorders of ‘higher’ (cortical) visual processing. In this review, we will draw together work from animal and human studies in an attempt to provide an insight into how Parkinson's disease affects the retina and how these changes might contribute to the visual symptoms experienced by patients.

Mechanisms of late-onset cognitive decline after early-life stress. - eScholarship

Abstract: Progressive cognitive deficits that emerge with aging are a result of complex interactions of genetic and environmental factors. Whereas much has been learned about the genetic underpinnings of these disorders, the nature of acquired contributing factors, and the mechanisms by which they promote progressive learning and memory dysfunction, remain largely unknown. Here, we demonstrate that a period of early-life psychological stress causes late-onset, selective deterioration of both complex behavior and synaptic plasticity: two forms of memory involving the hippocampus, were severely but selectively impaired in middle-aged, but not young adult, rats exposed to fragmented maternal care during the early postnatal period. At the cellular level, disturbances to hippocampal long-term potentiation paralleled the behavioral changes and were accompanied by dendritic atrophy and mossy fiber expansion. These findings constitute the first evidence that a short period of stress early in life can lead to delayed, progressive impairments of synaptic and behavioral measures of hippocampal function, with potential implications to the basis of age-related cognitive disorders in humans.

Vitamin E and cognitive decline in older persons.

Abstract: Background Previous studies raise the possibility that antioxidants protect against neurodegenerative diseases. Objective To examine whether intake of antioxidant nutrients, including vitamin E, vitamin C, and carotene, is associated with reduced cognitive decline with age. Design Longitudinal population-based study conducted from September 17, 1993, to November 20, 2000, with an average follow-up of 3.2 years. Patients The patients were 2889 community residents, aged 65 to 102 years, who completed a food frequency questionnaire, on average 18 months after baseline. Main Outcome Measure Cognitive change as measured by 4 tests (the East Boston Memory Test, which tests immediate and delayed recall; the Mini-Mental State Examination; and the Symbol Digit Modalities Test) at baseline and 3 years for all participants, and at 6 months for 288 randomly selected participants. Results We used random-effects models to estimate nutrient effects on individual change in the average score of the 4 cognitive tests. The cognitive score declined on average by 5.0 × 10 −2 standardized units per year. There was a 36% reduction in the rate of decline among persons in the highest quintile of total vitamin E intake (−4.3 × 10 −2 standardized units per year) compared with those in the lowest quintile (−6.7 × 10 −2 standardized units per year) ( P = .05), in a model adjusted for age, race, sex, educational level, current smoking, alcohol consumption, total calorie (energy) intake, and total intakes of vitamin C, carotene, and vitamin A. We also observed a reduced decline with higher vitamin E intake from foods ( P = .03 for trend). There was little evidence of association with vitamin C or carotene intake. Conclusion Vitamin E intake, from foods or supplements, is associated with less cognitive decline with age.

Dementia Three Months After Stroke Baseline Frequency and Effect of Different Definitions of Dementia in the Helsinki Stroke Aging Memory Study (SAM) Cohort

Abstract: Background and Purpose Vascular dementia is a common cause of dementia, and cerebrovascular disease is related to a higher risk of dementia. The frequency of dementia associated with ischemic stroke and the effects of different definitions of dementia in the diagnosis are still incompletely known. We evaluated the frequency of cognitive decline and dementia 3 months after ischemic stroke in a large stroke cohort. Methods Our cohort consisted of consecutively admitted ischemic stroke patients (n=486) aged 55 to 85 years in the Helsinki (Finland) Stroke Aging Memory Study (SAM). Subjects were assessed by structured medical, neurological, and radiological examinations and interview with a close informant, as well as by the Mini-Mental State Examination and detailed clinical mental status examination of defined cognitive domains. The criteria for dementia were those of the Diagnostic and Statistical Manual of Mental Disorders (DSM) (DSM-III, DSM-III-R, and DSM-IV), the National Institute of Neurological Disor...