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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
01 Sep 2010-Brain
TL;DR: Deep brain stimulation of the subthalamic nucleus is a safe procedure with regard to cognitive and behavioural morbidity over long-term follow-up, however, the global benefit partly decreases later in the course of the disease, due to progression of Parkinson's disease and the appearance of medication- and stimulation-resistant symptoms.
Abstract: Deep brain stimulation of the subthalamic nucleus represents the most important innovation for treatment of advanced Parkinson’s disease. Prospective studies have shown that although the beneficial effects of this procedure are maintained at 5 years, axial motor features and cognitive decline may occur in the long term after the implants. In order to address some unsolved questions raised by previous studies, we evaluated a series of 20 consecutive patients who received continuous stimulation for 8 years. The overall motor improvement reported at 5 years (55.5% at Unified Parkinson’s Disease Rating Scale—motor part, P50.001 compared with baseline) was only partly retained 3 years later (39%, P50.001, compared with baseline; 16.5%, P50.01, compared with 5 years), with differential effects on motor features: speech did not improve and postural stability worsened (P50.05). The preoperative levodopa equivalent daily dose was reduced by 58.2% at 5 years and by 60.3% at 8 years. In spite of subtle worsening of motor features, a dramatic impairment in functional state (56.6% at Unified Parkinson’s Disease Rating Scale—Activities of Daily Living, P50.01) emerged after the fifth year of stimulation. The present study did not reveal a predictive value of preoperative levodopa response, whereas few single features at baseline (such as gait and postural stability motor scores and the preoperative levodopa equivalent daily dose) could predict long-term motor outcome. A decline in verbal fluency (slightly more pronounced than after 5 years) was detected after 8 years. A significant but slight decline in tasks of abstract reasoning, episodic memory and executive function was also found. One patient had developed dementia at 5 years with further progression at 8 years. Executive dysfunction correlated significantly with postural stability, suggesting interplay between axial motor deterioration and cognition. Eight years after surgery, no significant change was observed on scales assessing depression or anxiety when compared with baseline. At 8 years, there was no significant increase of side-effects when compared with 5-year follow-up. In conclusion, deep brain stimulation of the subthalamic nucleus is a safe procedure with regard to cognitive and behavioural morbidity over long-term follow-up. However, the global benefit partly decreases later in the course of the disease, due to progression of Parkinson’s disease and the appearance of medication- and stimulation-resistant symptoms.

364 citations

Journal ArticleDOI
TL;DR: Preliminary support is provided that rosiglitazone may offer a novel strategy for the treatment of cognitive decline associated with AD, consistent with recent reports that plasma Abeta42 decreases with progression of AD.
Abstract: Objective Insulin resistance (impaired insulin action) has been associated with Alzheimer disease (AD) and memory impairment, independent of AD. Peroxisome proliferator-activated receptor-γ (PPAR-γ) agonists improve insulin sensitivity and regulate in-vitro processing of the amyloid precursor protein (APP). Authors evaluated the effects of the PPAR-γ agonist rosiglitazone on cognition and plasma levels of the APP derivative β-amyloid (Aβ) in humans. Methods In a placebo-controlled, double-blind, parallel-group pilot study, 30 subjects with mild AD or amnestic mild cognitive impairment were randomized to a 6-month course of rosiglitazone (4 mg daily; N=20) or placebo (N = 10). Primary endpoints were cognitive performance and plasma Aβ levels. Results Relative to the placebo group, subjects receiving rosiglitazone exhibited better delayed recall (at Months 4 and 6) and selective attention (Month 6). At Month 6, plasma Aβ levels were unchanged from baseline for subjects receiving rosiglitazone but declined for subjects receiving placebo, consistent with recent reports that plasma Aβ42 decreases with progression of AD. Conclusions Findings provide preliminary support that rosiglitazone may offer a novel strategy for the treatment of cognitive decline associated with AD. Future confirmation in a larger study is needed to fully demonstrate rosiglitazone's therapeutic potential.

364 citations

Journal ArticleDOI
TL;DR: To determine the association between vision and hearing impairment and subsequent cognitive and functional decline in community‐residing older women, a large sample of women aged 60 and over is studied.
Abstract: Author(s): Lin, Michael Y; Gutierrez, Peter R; Stone, Katie L; Yaffe, Kristine; Ensrud, Kristine E; Fink, Howard A; Sarkisian, Catherine A; Coleman, Anne L; Mangione, Carol M; Study of Osteoporotic Fractures Research Group | Abstract: ObjectivesTo determine the association between vision and hearing impairment and subsequent cognitive and functional decline in community-residing older womenDesignProspective cohort studySettingFour metropolitan areas of the United StatesParticipantsA total of 6,112 women aged 69 and older participating in the Study of Osteoporotic Fractures (SOF) between 1992 and 1994MeasurementsFive thousand three hundred forty-five participants had hearing measured, 1,668 had visual acuity measured, and 1,636 had both measured Visual impairment was defined as corrected vision worse than 20/40 Hearing impairment was defined as the inability to hear a tone of 40 dB or greater at 2,000 hertz Participants completed the modified Mini-Mental State Examination and/or a functional status assessment at baseline and follow-up Cognitive and functional decline were defined as the amount of decline from baseline to follow-up that exceeded the observed average change in scores by at least 1 standard deviationResultsAbout one-sixth (157%) of the sample had cognitive decline; 101% had functional decline In multivariate models adjusted for sociodemographic characteristics and chronic conditions, vision impairment at baseline was associated with cognitive (odds ratio (OR)=178, 95% confidence interval (CI)=121-261) and functional (OR=179, 95% CI=115-279) decline Hearing impairment was not associated with cognitive or functional decline Combined impairment was associated with the greatest odds for cognitive (OR=219, 95% CI=126-381) and functional (OR=187, 95% CI=101-347) declineConclusionSensory impairment is associated with cognitive and functional decline in older women Studies are needed to determine whether treatment of vision and hearing impairment can decrease the risk for cognitive and functional decline

364 citations

Journal ArticleDOI
TL;DR: In this article, the Subjective Cognitive Decline Initiative (SCD-I) published research criteria in the context of preclinical AD, with the aim of harmonization of SCD measurement across studies to enhance comparability and generalizability across studies.
Abstract: Introduction Subjective cognitive decline (SCD) manifesting before clinical impairment could serve as a target population for early intervention trials in Alzheimer's disease (AD). A working group, the Subjective Cognitive Decline Initiative (SCD-I), published SCD research criteria in the context of preclinical AD. To successfully apply them, a number of issues regarding assessment and implementation of SCD needed to be addressed. Methods Members of the SCD-I met to identify and agree on topics relevant to SCD criteria operationalization in research settings. Initial ideas and recommendations were discussed with other SCD-I working group members and modified accordingly. Results Topics included SCD inclusion and exclusion criteria, together with the informant's role in defining SCD presence and the impact of demographic factors. Discussion Recommendations for the operationalization of SCD in differing research settings, with the aim of harmonization of SCD measurement across studies are proposed, to enhance comparability and generalizability across studies.

363 citations

Journal ArticleDOI
TL;DR: Multiple epidemiological and animal model studies show that NSAIDs, the most widely used antiinflammatory agents, have a substantial sparing effect on AD and provide a proof of concept regarding the anti-inflammatory approach to disease modification.
Abstract: The amyloid cascade hypothesis is widely accepted as the centerpiece of Alzheimer disease (AD) pathogenesis. It proposes that abnormal production of beta amyloid protein (Abeta) is the cause of AD and that the neurotoxicity is due to Abeta itself or its oligomeric forms. We suggest that this, in itself, cannot be the cause of AD because demonstrating such toxicity requires micromolar concentrations of these Abeta forms, while their levels in brain are a million times lower in the picomolar range. AD probably results from the inflammatory response induced by extracellular Abeta deposits, which later become enhanced by aggregates of tau. The inflammatory response, which is driven by activated microglia, increases over time as the disease progresses. Disease-modifying therapeutic attempts to date have failed and may continue to do so as long as the central role of inflammation is not taken into account. Multiple epidemiological and animal model studies show that NSAIDs, the most widely used antiinflammatory agents, have a substantial sparing effect on AD. These studies provide a proof of concept regarding the anti-inflammatory approach to disease modification. Biomarker studies have indicated that early intervention may be necessary. They have established that disease onset occurs more than a decade before it becomes clinically evident. By combining biomarker and pathological data, it is possible to define six phases of disease development, each separated by about 5 years. Phase one can be identified by decreases in Abeta in the CSF, phase 2 by increases of tau in the CSF plus clear evidence of Abeta brain deposits by PET scanning, phase 3 by slight decreases in brain metabolic rate by PET-FDG scanning, phase 4 by slight decreases in brain volume by MRI scanning plus minimal cognitive impairment, phase 5 by increased scanning abnormalities plus clinical diagnosis of AD, and phase 6 by advanced AD requiring institutional care. Utilization of antiinflammatory agents early in the disease process remains an overlooked therapeutic opportunity. Such agents, while not preventative, have the advantage of being able to inhibit the consequences of both Abeta and tau aggregation. Since there is more than a decade between disease onset and cognitive decline, a window of opportunity exists to introduce truly effective disease-modifying regimens. Taking advantage of this opportunity is the challenge for the future.

363 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