Cognitive decline

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

Cognitive Impairment in Huntington Disease: Diagnosis and Treatment

Abstract: Cognition has been well characterized in the various stages of Huntington disease (HD) as well as in the prodrome before the motor diagnosis is given. Although the clinical diagnosis of HD relies on the manifestation of motor abnormalities, the associated impairments have been growing in prominence for several reasons. First, research to understand the most debilitating aspects of HD has suggested that cognitive and behavioral changes place the greatest burden on families, are most highly associated with functional decline, and can be predictive of institutionalization. Second, cognitive impairments are evident at least 15 years prior to the time at which motor diagnosis is given. Finally, cognitive decline is associated with biological markers such as brain atrophy, circulating levels of brain-derived neurotrophic factors, and insulin-like growth factor 1. Efforts are now underway to develop valid and reliable measures of cognition in the prodrome as well as in all stages of HD so that clinical trials can be conducted using cognitive outcomes.

The neurobiological basis of cognitive impairment in Parkinson's disease.

Abstract: The recent formalization of clinical criteria for Parkinson's disease with dementia (PDD) codifies many studies on this topic, including those assessing biological correlates. These studies show that the emergence of PDD occurs on the background of severe dopamine deficits with, the main pathological drivers of cognitive decline being a synergistic effect between alpha-synuclein and Alzheimer's disease pathology. The presence of these pathologies correlates with a marked loss of limbic and cortically projecting dopamine, noradrenaline, serotonin, and acetylcholine neurons, although the exact timing of these relationships remains to be determined. Genetic factors, such as triplications in the α-synuclein gene, lead to a clear increased risk of PDD, whereas others, such as parkin mutations, are associated with a reduced risk of PDD. The very recent formalization of clinical criteria for PD with mild cognitive impairment (PD-MCI) allows only speculation on its biological and genetic bases. Critical assessment of animal models shows that chronic low-dose MPTP treatment in primates recapitulates PD-MCI over time, enhancing the current biological concept of PD-MCI as having enhanced dopamine deficiency in frontostriatal pathways as well as involvement of other neurotransmitter systems. Data from other animal models support multiple transmitter involvement in cognitive impairment in PD. Whereas dopamine dysfunction has been highlighted because of its obvious role in PD, the role of the other neurotransmitter systems, neurodegenerative pathologies, and genetic factors in PD-MCI remains to be fully elucidated.

Intellectual Deficits in First-Episode Schizophrenia: Evidence for Progressive Deterioration

Abstract: The developmental processes leading to neuropsychological deficits in schizophrenia are poorly understood. Both early developmental defects and subsequent deterioration may occur. Intelligence test profiles are often used to estimate premorbid ability and deterioration from prior levels of functioning. These characteristics were assessed in samples of firstepisode (« = 51) and chronic (« = 50) schizophrenic patients. Although the groups showed few differences on tests to estimate premorbid intellectual ability, the chronic group performed worse on measures considered sensitive to deterioration. Dextral (right-handed) patients tended to have better performance; this effect was marked in the firstepisode sample, especially on verbal tests. Male patients showed more evidence of deterioration than female patients. Subgroups differing in the time course of premorbid social dysfunction also differed in intelligence test profiles, suggesting that estimates of social and cognitive deterioration may have concurrent validity. The results support the hypothesis that patients differ in the course of cognitive decline and suggest that deterioration of function may follow the onset of overt psychosis in some patients. Prospective longitudinal studies of first-episode schizophrenic patients could directly test this hypothesis.

Educational attainment and cognitive decline in old age

Abstract: Risk of dementia and Alzheimer disease (AD) in old age is reduced in persons with higher levels of educational attainment compared to those with lower levels.1–4 This finding is due in part to the well-established correlation of education with cognitive test performance at all ages. Thus, persons with more schooling, relative to those with less, are likely to begin old age at a higher level of cognitive function and so would need to experience more cognitive decline before reaching a level of impairment meeting dementia criteria. Another way in which education might influence risk of dementia is by a correlation with late life cognitive decline, the primary clinical manifestation of AD. Consistent with this idea, several studies have reported an association of higher educational attainment with reduced cognitive decline.5–23 However, this research is mostly based on change between two measurement points. Although this approach can provide an estimate of rate of change in cognitive function, it has a fundamental limitation: even with statistical adjustments, change in function between two time points is hard to securely distinguish from level of function at either point.24 This limitation is especially telling when the predictor of interest is highly correlated with the outcome as in the present case. Importantly, therefore, such studies are not well positioned to separate the estimate of education’s correlation with cognitive decline from its strong correlation with level of cognition. Assessment of cognition at three or more points in time permits separation of initial level of cognition from rate of change, but fewer of these studies have been published and their findings on the relation of higher educational attainment to cognitive decline have been mixed.12,17,19,21,25–28 Other factors may be contributing to this inconsistency. For example, education has been quantified in different ways (e.g., categorically vs continuously, linearly vs nonlinearly) and its association with cognitive decline may be modified by other variables (e.g., preexisting cognitive impairment, practice effects, race/ethnicity). In the present study, we test the hypothesis that higher level of education is associated with reduced rate of cognitive decline in old age using data from the Chicago Health and Aging Project, a longitudinal population-based study of aging and AD. Participants are more than 6,000 older African American and white residents of a community on the south side of Chicago. At approximately 3-year intervals for up to 14 years, they completed four brief tests of cognitive performance from which a previously established composite measure of global cognition was derived. We used mixed-effects models to characterize person-specific paths of cognitive change and to test the relation of education to initial level of cognition and annual rate of change. In subsequent analyses, we examined other socioeconomic indicators and tested whether the association of education with change in cognitive function was modified by race, cognitive impairment, or repeated exposure to the cognitive tests.

Montreal Cognitive Assessment Performance in Patients with Parkinson’s Disease with “Normal” Global Cognition According to Mini-Mental State Examination Score

Abstract: Cognitive impairment insufficient to meet criteria for dementia (mild cognitive impairment (MCI)) has been reported to occur in 20% to 30% of patients with Parkinson’s disease (PD),1–5 even in newly diagnosed patients.4,5 Identification of initial impact or MCI in PD is important, because it predicts future cognitive decline, including development of PD dementia (PDD),2,3,6,7 and deterioration of health-related quality of life.8 Impairments in executive function, attention, visuospatial skills, and memory characterize the “typical” cognitive profile in PD, whereas language and praxis are thought to be relatively spared.3,4,9 The memory impairment associated with PD is classically considered a retrieval deficit (i.e., subcortical memory profile) as opposed to an encoding deficit (i.e., cortical memory profile). There is substantial overlap in the pattern of observed cognitive deficits in PD without dementia and PDD. Studies enrolling both groups of patients have shown qualitatively similar, but quantitatively greater, impairments in patients with PDD in executive function, visuospatial abilities, attention, and psychomotor skills.10 In longitudinal studies of patients without dementia at baseline, verbal memory deficits11 and executive or visuospatial impairments12 have been shown to predict development of PDD on long-term follow-up. Given the aforementioned high prevalence of MCI in PD and its association with future development of dementia, it is important that patients with PD, even those with mild disease, be screened regularly for cognitive impairment.12 An ideal cognitive screening instrument in PD should be brief, assess a range of cognitive domains, simple to administer, sensitive to the initial stage of cognitive impairment, and unaffected by motor impairment. Few screening instruments have been validated or developed to assess global cognition in PD. The Scales for Outcomes of Parkinson’s Disease—Cognition was recently developed and has been shown to be valid and reliable in differentiating patients with PD with and without dementia,13,14 but its performance, specifically in patients without significant global cognitive impairment, has not been reported. The Cambridge Cognitive Examination—Revised distinguishes between patients with PD with and without dementia and detects cognitive impairment in patients with PD with an MMSE score less than 25,15 but it takes approximately 60 minutes to administer. The Mini-Mental State Examination (MMSE)16 remains the most commonly used screening instrument for global cognition. The MMSE is used extensively in PD, but its use in this population has been questioned,17,18 in part because the MMSE primarily assesses memory and language skills and also may not be sensitive to detect many cases of MCI. The Montreal Cognitive Assessment (MoCA)19 is a new cognitive screening instrument that was designed to address some of the limitations of the MMSE. It assesses a broader range of cognitive domains than the MMSE and is more challenging from a cognitive standpoint overall. The MoCA and the MMSE both have items that require motor skills that core PD symptoms potentially affect (5/30 points on the MoCA and MMSE). The MoCA has been shown to be more sensitive than the MMSE for the detection of MCI and mild Alzheimer’s disease in the general population, and a score less than 26 was found to be the optimal cutoff point for a diagnosis of cognitive impairment.19 There have been two studies using the MoCA in PD, and in one, the MoCA was found to be more sensitive than the MMSE in detecting cognitive impairment in this population,17 although a MMSE score less than 26 was used to classify patients as having cognitive impairment, and this cutoff has not been validated for PD. In addition, the authors did not examine differences in MoCA subscores in impaired and unimpaired groups or examine correlates of MoCA performance. In the other study, the MoCA was found to have good test–retest reliability, interrater reliability, and convergent validity with a neuropsychological battery in a small sample of patients with PD.20 This study presents results on the frequency and correlates of cognitive impairment using the MoCA in patients with PD. These patients were a priori defined as not meeting criteria for global cognitive impairment when evaluated with the MMSE. It was hypothesized that a substantial proportion of patients with PD would be impaired (score <26) on the MoCA in spite of having a normal MMSE score and that cognitive impairment would occur in a range of domains, including visuospatial and executive abilities, attention, and memory.