Relevant bibliographies by topics / Cognitive decline

Academic literature on the topic 'Cognitive decline'

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Published: 4 June 2021
Last updated: 9 March 2023

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Journal articles on the topic "Cognitive decline"

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Tomaszewski Farias, Sarah, Tania Giovannetti, Brennan R. Payne, Michael Marsiske, George W. Rebok, K. Warner Schaie, Kelsey R. Thomas, et al. "Self-perceived Difficulties in Everyday Function Precede Cognitive Decline among Older Adults in the ACTIVE Study." Journal of the International Neuropsychological Society 24, no. 1 (August 11, 2017): 104–12. http://dx.doi.org/10.1017/s1355617717000546.

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AbstractObjectives: Careful characterization of how functional decline co-evolves with cognitive decline in older adults has yet to be well described. Most models of neurodegenerative disease postulate that cognitive decline predates and potentially leads to declines in everyday functional abilities; however, there is mounting evidence that subtle decline in instrumental activities of daily living (IADLs) may be detectable in older individuals who are still cognitively normal. Methods: The present study examines how the relationship between change in cognition and change in IADLs are best characterized among older adults who participated in the ACTIVE trial. Neuropsychological and IADL data were analyzed for 2802 older adults who were cognitively normal at study baseline and followed for up to 10 years. Results: Findings demonstrate that subtle, self-perceived difficulties in performing IADLs preceded and predicted subsequent declines on cognitive tests of memory, reasoning, and speed of processing. Conclusions: Findings are consistent with a growing body of literature suggesting that subjective changes in everyday abilities can be associated with more precipitous decline on objective cognitive measures and the development of mild cognitive impairment and dementia. (JINS, 2018, 24, 104–112)
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Fonseca, Jose Andres Saez, Rhiannon Ducksbury, Joanne Rodda, Timothy Whitfield, Chitra Nagaraj, Kallur Suresh, Tim Stevens, and Zuzana Walker. "Factors that predict cognitive decline in patients with subjective cognitive impairment." International Psychogeriatrics 27, no. 10 (March 27, 2015): 1671–77. http://dx.doi.org/10.1017/s1041610215000356.

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ABSTRACTBackground:Current evidence supports the concept of a preclinical phase of Alzheimer's disease (AD) where pathological and imaging changes are present in asymptomatic individuals. Subjective cognitive impairment (SCI) may represent the earliest point on the continuum of AD. A better understanding of the baseline characteristics of this group of patients that later decline in cognition will enhance our knowledge of the very early disease processes, facilitate preventive strategies, early diagnosis, timely follow-up and treatment.Methods:An observational exploratory study which followed up 62 consecutive patients with SCI presenting to a memory clinic and compared baseline characteristics of SCI patients who declined cognitively with those who did not. Cognitive decline was defined as a progression to a diagnosis of amnestic mild cognitive impairment (aMCI) or dementia at follow-up.Results:Patients were followed up for a mean of 44 months (range 12–112 months). At the time of follow up, 24% of patients had declined. Patients that declined were significantly older at onset of symptoms and first presentation to memory clinic, and took significantly more medications for physical illnesses. Patients that declined also performed significantly worse on Trail Making Test (TMT) B and Cambridge Cognitive Examination – Revised (CAMCOG-R) at baseline. Survival analysis identified key variables that predicted decline (later age of onset and later age at first assessment).Conclusions:Patients who present with subjective memory complaints and are over the age of 61 years are at high risk of cognitive decline and warrant an in-depth assessment and follow-up.
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Kaufmann, Christopher N., Mark W. Bondi, James D. Murphy, Xin Tu, and Alison A. Moore. "COGNITIVE TRAJECTORIES BEFORE AND AFTER SLEEP TREATMENT INITIATION IN U.S. OLDER ADULTS WITH SLEEP DISTURBANCE." Innovation in Aging 3, Supplement_1 (November 2019): S403—S404. http://dx.doi.org/10.1093/geroni/igz038.1499.

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Abstract Sleep disturbances are associated with cognitive decline but it is not clear if initiation of sleep treatments mitigates decline. We used the 2006-2014 Health and Retirement Study. At each wave, participants were administered cognitive assessments and scores were summed (values=0-35; higher=better cognition). All participants also reported if, in the past two weeks, they had taken medications or used other treatments to improve sleep. Our sample (N=4,650) included individuals who at baseline were cognitively normal and untreated for sleep, and at any wave reported some sleep disturbance. We characterized cognitive performance over study period with comparisons before and after sleep treatment initiation. Between 2006-2014, participants exhibited declines in cognitive performance (B=-2.40; 95% CI=-2.73, -2.06; p<0.001) after controlling for confounders. Following sleep treatment, cognitive decline became less pronounced (interaction B=0.94; 95% CI=0.21, 1.67; p=0.013). Results suggest that in older adults with sleep disturbance, initiation of sleep treatment may slow cognitive decline.
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Fernandez, Shane, Samantha C. Burnham, Lidija Milicic, Greg Savage, Paul Maruff, Madeline Peretti, Hamid R. Sohrabi, et al. "SPON1 Is Associated with Amyloid-β and APOE ε4-Related Cognitive Decline in Cognitively Normal Adults." Journal of Alzheimer's Disease Reports 5, no. 1 (February 24, 2021): 111–20. http://dx.doi.org/10.3233/adr-200246.

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Abstract. Background: Genetic variation in Spondin-1, specifically rs11023139, has been associated with reduced rates of cognitive decline in individuals with Alzheimer’s disease. Objective: The aim of this study was to assess whether the association was present in cognitively normal older adults. Methods: Longitudinal cognitive decline was investigated using linear mixed modelling in a cohort of 590 cognitively normal older adults enrolled in the Australian Imaging, Biomarkers and Lifestyle Study. Results: No independent effect of Spondin-1 rs11023139 on cognitive decline was observed. However, significant associations were observed for the interaction between Apolipoprotein E (APOE) ɛ4 and rs11023139 in individuals with high amyloid-β burden. APOE ɛ4/rs11023139-A carriers declined significantly faster than APOE ɛ4/rs11023139-G_G carriers in measures of global cognition (p = 0.011) and verbal episodic memory (p = 0.020). Conclusion: These results suggest that carriage of the Spondin-1 rs11023139-A allele significantly contributes to a worsening of cognitive performance in APOE ɛ4 cognitively normal older adults with a high neocortical amyloid-β burden.
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Stieger, Mirjam, and Margie Lachman. "Cognitive Activity as a Moderator of Educational Attainment and Work Status in Cognitive Aging." Innovation in Aging 4, Supplement_1 (December 1, 2020): 290–91. http://dx.doi.org/10.1093/geroni/igaa057.931.

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Abstract Cross-sectional findings showed that education differences in memory performance were moderated by frequent cognitive activity (Lachman et al., 2010). The present study examined whether frequent cognitive activity could compensate for lower education when focusing on change in cognitive performance across nine years. The study also explored whether cognitive activity can slow down declines in retired adults as previous research suggested that retiring is associated with an increased risk of cognitive decline (e.g., Wickrama et al., 2013). Longitudinal data from the MIDUS study included N = 3,325 middle-aged and older adults. Outcome variables were two factors of cognitive performance: Episodic Memory (EM) and Executive Functioning (EF). Independent variables were years of education, work status (working vs. retired), and frequency of cognitive activity. The results suggest that cognitive activity moderated the effect of educational attainment on change in EM. Individuals with both higher education and cognitive activity showed the smallest declines in EM. Individuals with lower educational attainment but high cognitive activity had less decline in EM compared to their low education counterparts. Those who increased their cognitive activity over time showed less decline in EF. In terms of work status, working adults had less decline in EM and EF compared to retired adults and retired adults who did not maintain their cognitive activity declined more in EF. The results emphasize the importance of frequent engagement in cognitive activity across the lifespan, which can attenuate cognitive declines especially among those who have lower education or have retired.
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Kiselica, A., J. Benge, A. Kaser, B. Small, and T. Webber. "A-01 Objective and Subjective Cognitive Declines as Complementary Symptoms of Early Alzheimer’s Disease." Archives of Clinical Neuropsychology 35, no. 6 (August 28, 2020): 774. http://dx.doi.org/10.1093/arclin/acaa067.01.

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Abstract Objective Subjective and objective cognitive declines are given equal weight as symptoms of pre-mild cognitive impairment in Alzheimer’s disease by recent research criteria. However, the overlap of these constructs is unclear. We used standardized regression-based (SRB) change to define subtle objective cognitive decline across serial neuropsychological assessments. We then examined the associations between objective change and subjective cognitive complaints. Finally, we investigated the impact of different symptom combinations on rates of classification for the early stages of the Alzheimer’s Continuum. Method Data from 1,341 cognitively intact older adults with serial Uniform Data Set 3.0 Neuropsychological Battery assessments (6–24-month follow-ups) were used to compute SRB declines at the following z-scores cut-points: −1.282, −1.645, and − 1.96. We used Chi-square tests and Cohen’s kappa statistics to evaluate the relationship between SRB change and presence/absence of subjective cognitive decline at follow-up. We also examined the prevalence rates of different symptom combinations in an amyloid positive sample (n = 29). Results The base rate of having at least one significant SRB decline ranged from 26.00% to 59.40%. Subjective cognitive decline was positively associated with SRB-defined decline in the normative sample, though agreement was limited (= − .01–.10). SRB decline with no subjective decline occurred in 0.0–37.90% of amyloid positive participants, while 3.40–37.90% had subjective but not objective decline. 37.90–79.30% of amyloid positive participants exhibited either SRB or subjective decline. Conclusions Subjective and objective cognitive declines appear to represent unique symptom classes and should be separately considered when staging patients on the Alzheimer’s Continuum.
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Dasgupta, Indranil, Mitesh Patel, Nuredin Mohammed, Jyoti Baharani, Thejasvi Subramanian, G. Neil Thomas, and George Tadros. "Cognitive Function Declines Significantly during Haemodialysis in a Majority of Patients: A Call for Further Research." Blood Purification 45, no. 4 (2018): 347–55. http://dx.doi.org/10.1159/000485961.

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Introduction: Cognitive impairment (CI) is very common condition that occurs in haemodialysis patients and it is associated with reduced functional capacity and mortality. We assessed the change in cognitive function during haemodialysis and associated risk factors. Methods: All patients ≥50 years, on haemodialysis for ≥3 months, no dementia from 2 dialysis centres were selected. Cognition was assessed before and after a haemodialysis session using parallel versions of the Montreal Cognitive Assessment (MOCA) tool. Multiple regression was used to examine potential confounders. Results: Eight-two patients completed both tests – median age 73 (52–91) years, 59% male, dialysis vintage 41 (3–88) months. Sixty-two (76%) had CI at baseline. Cognition declined over dialysis (MOCA 21 ± 4.8 to 19.1 ± 4.1, p < 0.001) and domains affected were attention, language, abstraction and delayed recall. Age and dialysis vintage were independently associated with decline. Conclusion: Cognitive function declines over a haemodialysis session and this has significant clinical implications over health literacy, self-management and tasks like driving. More research is needed to find the cause for this decline in cognition.
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Atkinson, Taylor, Dylan Jester, and William Haley. "Spousal Caregiving and Cognitive Trajectories: Does Care Recipient Dementia Status Matter?" Innovation in Aging 4, Supplement_1 (December 1, 2020): 359–60. http://dx.doi.org/10.1093/geroni/igaa057.1157.

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Abstract Caregiving is often considered stressful, even more so if the care recipient has been diagnosed with dementia. The current study examines the rate of cognitive decline of spousal caregivers of persons with dementia (CG-D) when compared to spousal caregivers of persons without dementia (CG) before and after the death of the care recipient. Health and Retirement Study (HRS) data from 1998-2016 were used to examine cognitive trajectories of CG-D (n=364) and CG (n=1,649) before and after the care recipient death. Cognition was measured through the HRS’s shortened Telephone Interview of Cognitive Status and separated into measures of total cognition and memory. Covariates included age, education, sex, race, ethnicity, care hours, frailty, socioeconomic status, nursing home placement of the recipient, and whether the death was expected. Piecewise mixed models were constructed to examine two two-year periods of decline leading up to the death of the care recipient, and two two-year periods of decline after the death of the care recipient. CG-D and CG declined at equivalent rates on measures of total cognition and memory (ps &gt; .05). In all caregivers, total cognition and memory declined at a stable rate before the death of the care recipient. However, an accelerated decline was evident after the death of the care recipient (ps &lt; .001). Our results suggest that cognitive decline is not differentially affected by care recipient dementia diagnosis. We find evidence that the death of a spousal care recipient is accompanied by hastened cognitive decline in our population-based sample.
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Tales, Andrea, Frank Jessen, Christopher Butler, Gordon Wilcock, Judith Phillips, and Tony Bayer. "Subjective Cognitive Decline." Journal of Alzheimer's Disease 48, s1 (September 24, 2015): S1—S3. http://dx.doi.org/10.3233/jad-150719.

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Sander, Ruth. "Detecting cognitive decline." Nursing Older People 24, no. 2 (February 24, 2012): 13. http://dx.doi.org/10.7748/nop.24.2.13.s11.

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Dissertations / Theses on the topic "Cognitive decline"

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Hogervorst, Eva. "Age-related cognitive decline and cognition enhancers." Maastricht : Maastricht : Neuropsych Publishers ; University Library, Maastricht University [Host], 1998. http://arno.unimaas.nl/show.cgi?fid=6058.

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McAulay, Vincent. "Cognitive decline during acute hypoglycaemia." Thesis, University of Edinburgh, 2006. http://hdl.handle.net/1842/24922.

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The initial chapters of this thesis describe the clinical and physiological aspects of hypoglycaemia, followed by a review of the literature on the effects of acute hypoglycaemia on cognitive function. The subsequent chapters describe original research studies in subjects with and without diabetes, which examine the effects of acute hypoglycaemia on aspects of cognitive function and the prevention of hypoglycaemia. In Studies 1 to 3, a hyperinsulinemic glucose clamp was used to either maintain euglycemia (blood glucose 4,5 mmol/l) or induce hypoglycaemia (2.6 mmol/l) in both healthy adults (n=20), and subjects with type 1 diabetes (n=16). A cognitive test battery was administered to examine aspects of attention, intelligence, motivation, affect and subjective cognition. Hypoglycaemia induced a significant deterioration in tests sensitive to both visual and auditory selective attention, and attentional flexibility deteriorated (Studies 1 and 2). Intelligence scores did not deteriorate during hypoglycaemia (Studies 1 and 2). In Study 3, hypoglycaemia increased task-irrelevant interference and self-focus of attention, but motivation declined to a similar extent during both study conditions. Hypoglycaemia produced a negative mood state with a significant fall in energy levels and a concomitant rise in anxiety (Study 3). Study 4 was an open-label, comparative study of the post-prandial glucodynamics of insulin lispro, when administered either 5 minutes before or 20 minutes after a high fat/high solid phase meal, in twelve subjects with type 1 diabetes. Administration of insulin lispro after the meal reduced the risk of early postprandial hypoglycaemia, without compromising postprandial glycaemic control. Therefore, the work in this thesis has demonstrated a different deterioration of attentional function in humans during hypoglycaemia with no effect on non-verbal reasoning skills. Furthermore, it would appear that the brain is not only less cognitively competent and more dysphoric during hypoglycaemia, it is also more self-aware and distracted when required to perform effortful processing.
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De, Marco Matteo. "Cognitive and physical stimulation, genetic risk and cognitive decline." Thesis, University of Sheffield, 2012. http://etheses.whiterose.ac.uk/3379/.

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Miralbell, Blanch Júlia. "Biomarkers of cognitive decline and dementia." Doctoral thesis, Universitat de Barcelona, 2012. http://hdl.handle.net/10803/91068.

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Cognitive impairment in the elderly encompasses many forms, ranging from subtle impairments in otherwise cognitively healthy individuals through mild cognitive impairment and dementia. Brain structural and functional changes underlie the observed cognitive impairment. Complementary to the clinical observation, biomarkers have been proposed as in vivo indicators of the underlying pathophysiology and neurobiological changes in a sufficiently reliable manner that they could be used to detect, track, and predict the disease course over time. In this thesis we used a combination of epidemiological and clinic-based approaches to investigate the mechanisms underlying vascular cognitive impairment (VCI) and Alzheimer’s disease (AD) and to identify possible biomarkers that could help early diagnosis of such conditions. To do so, a set of circulating and cerebrospinal fluid (CSF) biomarkers were studied in healthy and cognitively impaired subjects. Then, these measures were related to grey matter (GM) volumes, white matter (WM) integrity and cognition. The first two studies are part of the population-based Barcelona-ASIA neuropsychology study. Study I aimed to compare the cognitive patterns of risk markers for cerebrovascular disease (CVD) with the cognitive profile in relation to novel and traditional vascular risk factors (VRF) in a community-dwelling sample. Biomarkers of inflammation, endothelial dysfunction and vascular thrombosis were selected. Results showed that VRF and circulating markers of inflammation and endothelial dysfunction predicted performance in several cognitive domains. Cognitive patterns of inflammatory markers overlapped those related to VRF. Markers of endothelial dysfunction predicted lower performance in verbal memory. Study II was designed to further explore the structural changes mediating the relationships between risk markers of CVD and cognition. For that purpose the same set of markers of risk for CVD were related to GM atrophy and WM integrity and cognition. The main finding was an association of inflammation and vascular thrombosis with WM integrity loss in cortico-subcortical pathways and association fibres of frontal and temporal lobes. As expected, none of the biomarkers was related to GM volume changes. Vascular thrombosis also predicted lower performance in processing speed. The third study is a memory clinic-based investigation that was conducted aiming to test the potential use of CSF biomarkers cut-offs as components for the diagnostic work-up in AD. We assessed GM and cognitive patterns in cognitively impaired subjects using CSF Aβ1-42, t-tau and p-tau181 cut-offs as grouping criteria. Results indicated that patients with abnormal CSF levels of t-tau and p-tau (but not Aβ1-42) showed impairment and signs of regional GM atrophy in brain regions characteristic for AD, compared to those with normal levels. More specifically, GM volume differences were found in temporal, inferior parietal, lateral occipital and widespread prefrontal regions. Studies I and II show that risk markers of inflammation and vascular thrombosis are related to a VCI profile for both cognitive patterns and structural brain changes. A microvascular damage of WM projections in fronto-subcortical pathways, but not GM atrophy, could mediate the association between these pathogenic processes and cognitive performance. Markers of endothelial dysfunction are related to a different cognitive pattern which is characteristic of both vascular and neurodegenerative mechanisms. Study III provides evidence that patients with abnormal CSF levels of t-tau and p-tau (but not Aβ1-42) show cognitive an AD profile according to GM density patterns and cognitive impairment. Taken together, these results suggest that, complementary to the clinical observation, plasma and CSF markers and structural imaging are well placed to improve early diagnosis of both VCI and AD.
El terme deteriorament cognitiu (DC) es refereix al contínuum de canvis cognitius associats a l’envelliment sa i patològic. El diagnòstic precoç de les persones amb DC és clau, ja que els tractaments són més eficaços quan s’inicien als inicis de la malaltia. Els biomarcadors s’han proposat com a eines pel diagnòstic precoç del DC i la demència. Es consideren indicadors in vivo de la patologia i s’han plantejat com a possibles eines pel diagnòstic, pronòstic i seguiment del DC i la patologia subjacent. L’objectiu general de la present tesi era explorar els mecanismes patofisiològics subjacents al deteriorament cognitiu vascular (DCV) i la (MA). Per aquest motiu, vàrem mesurar diversos biomarcadors sanguinis i de LCR en persones sanes i en persones amb diagnòstic de deteriorament cognitiu i vàrem relacionar-los amb canvis de l’estructura cerebral i de la cognició. L’objectiu final era identificar possibles biomarcadors pel diagnòstic precoç d’aquestes malalties. Els estudis I i II s’emmarquen dins del projecte Barcelona-ASIA Neuropsicologia i tenien com a objectiu estudiar la relació entre biomarcadors en plasma de malaltia vascular cerebral (MVC) i canvis estructurals i cognitius. Els resultats obtinguts mostren que els biomarcadors d’inflamació i trombosi vascular es relacionen amb un perfil de deteriorament cognitiu vascular tant a nivell cognitiu com estructural. La lesió microvascular dels tractes de SB còrtico-subcorticals mediaria l’associació entre aquests mecanismes i la cognició. Els marcadors de disfunció endotelial es relacionen amb un perfil cognitiu diferent, que és característic tant de processos vasculars com neurodegeneratius. L’estudi III té com a objectiu valorar el possible ús dels biomarcadors de líquid cefaloraquidi pel diagnòstic de la MA. En concret, vàrem estudiar els perfils estructurals i cognitius en persones amb deteriorament cognitiu emprant punts de tall de líquid cefaloraquidi com a criteri d’agrupació. Els resultats mostren que pacients amb DC i amb nivells patològics de t-tau i p-tau al LCR (però no d’Aβ1-42) presenten un perfil cognitiu i estructural de MA. En conclusió, els resultats obtinguts en la present tesi suggereixen que, complementaris a l’observació clínica, els biomarcadors de LCR i plasma, així com els indicadors de morfologia cerebral podrien ser d’ús pel diagnòstic precoç del DCL i la demència.
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Lu, Zhengdong. "Constrained clustering and cognitive decline detection /." Full text open access at:, 2008. http://content.ohsu.edu/u?/etd,650.

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Marston, Kieran John. "Preventing cognitive decline through resistance training." Thesis, Marston, Kieran John (2019) Preventing cognitive decline through resistance training. PhD thesis, Murdoch University, 2019. https://researchrepository.murdoch.edu.au/id/eprint/51337/.

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The foundations for later-life cognitive health are often laid decades prior to the first symptoms of cognitive decline, therefore preventative strategies should be implemented early in life. Structured resistance training shows promise at reducing dementia risk and has been associated with enhanced cognitive function and biomarker profiles. More specifically, intense acute resistance exercise and chronic resistance training may increase levels of growth factors, such as brain-derived neurotrophic factor (BDNF), insulin-like growth factor (IGF-1) and vascular endothelial growth factor (VEGF), which influence the proliferation and maintenance of neural and vascular tissue. Furthermore, biomarkers associated with suboptimal cognitive health (e.g., homocysteine) are decreased following longer-term resistance training. Although promising, the current literature is inconsistent, with varying resistance exercise regimens implemented, contributing to conflicting reported effects on cognition and biomarkers. The aim of the current thesis was to evaluate the impact of different strength training protocols on cognitive health. Four studies were conducted to examine acute response in growth factors following resistance exercise in young and older adults, and the chronic response in neurotrophic growth factors and cognitive function following resistance training in older adults. Chapters Four and Five explored the acute response in neurotrophic growth factors to intense resistance exercise in young or late middle-aged adults. Sixteen young adults were recruited (Chapter Four) to perform to-fatigue (i.e., maximal), high-volume acute resistance exercise bouts: i) traditional hypertrophy-based resistance exercise (i.e., three sets, 10 repetitions at 100% of 10 repetition maximum [RM]), or ii) traditional strength-based resistance exercise (i.e., five sets, five repetitions at 100% of 5RM). Levels of serum BDNF and blood lactate concentration (i.e., physiological marker of session intensity) were measured prior to and following exercise. Serum BDNF was increased (p<0.01; d=0.52) immediately post-hypertrophy resistance exercise when compared to strength resistance exercise. Change in serum BDNF levels were positively correlated (r=0.70; p<0.01) with change in blood lactate concentration immediately following hypertrophy-based resistance exercise only. The acute BDNF response to resistance exercise may not be consistent across the lifespan, and to-fatigue and high-volume resistance exercise is not practical in ageing adults. For this reason, Chapter Five explored the acute growth factor response to intense, yet pragmatic resistance exercise (i.e., submaximal and lower-volume) in 29 late middle-aged adults. Two resistance exercise sessions i) moderate-load (i.e., three sets, 10 repetitions at 70% of 1RM), or ii) high-load (i.e., five sets, five repetitions at 85% of 1RM) were performed in parallel groups (Chapter Six and Seven). Session intensity was determined by change in blood lactate concentration, and session rating of perceived exertion (sRPE). Serum samples were taken prior to and following exercise for later BDNF, IGF-1, and VEGF analysis. No acute changes in BDNF, IGF-1 or VEGF were observed. Changes in BDNF, IGF-1 or VEGF were not associated with changes in blood lactate concentration or sRPE. My findings provide evidence that to-fatigue, high-volume resistance exercise can increase acute levels of BDNF; however, under more practical resistance training scenarios (e.g., moderate volume, submaximal resistance exercise) this outcome is less likely to occur. Resting levels of BDNF, IGF-1, VEGF and homocysteine are important predictors for later life cognitive function in ageing adults; thus, Chapter Six explored changes in resting blood markers following a 12-week period of intense, lower-volume resistance training twice per week in 45 late middle-aged adults. Participants were randomised into one of three groups; i) moderate-load (i.e., three sets, 10 repetitions at 70% of 1RM), ii) high-load (i.e., five sets, five repetitions at 85% of 1RM), or iii) a non-exercising (i.e., no intervention) control group for comparison. Fasted levels of serum BDNF, IGF-1, VEGF, and plasma homocysteine were quantified from blood samples collected before and after the 12-week intervention. No differences were observed in BDNF, IGF-1, VEGF, or plasma homocysteine from pre- to post- intervention between groups. Despite an intense training stimulus, it is possible that the protocols implemented here were not of high enough volume to enhance growth factors. However, high-intensity and high-volume resistance exercise is not a practical training model in ageing adults. Chapters Four-Six placed a strong emphasis on the importance of physiology, and the levels of certain biomarkers, in regards to cognitive health. Therefore, it is essential to evaluate the functional outcomes of resistance training on cognitive health. As part of the randomised controlled trial introduced in Chapter Six, Chapter Seven explored the response in cognitive function following 12 weeks of intense resistance training in 45 late middle-aged adults. Participants were randomised into either i) moderate-load resistance training, ii) high-load resistance training, or iii) a non-exercising control group. Cognitive function was assessed using the CogState computerised cognitive battery, which evaluates performance within several cognitive domains. Greater delayed short-term memory (p=0.02) was observed in high-load and moderate-load groups when compared to the control, with no difference observed between resistance training groups. No other differences for changes in cognitive function between groups were observed. In cognitively healthy adults, 12 weeks of intense resistance training enhances short-term memory, a finding supporting the use of structured resistance training to promote physical and cognitive health. In conclusion, the findings presented in this thesis provide evidence that resistance exercise needs to be to-fatigue and high in volume to enhance BDNF levels. Intense resistance exercise in late middle-aged adults influences neither the acute nor chronic response in neurotrophic growth factors or homocysteine when resistance exercise is reduced in total volume. However, 12 weeks of intense resistance training enhances short-term memory in cognitively healthy adults, a relevant outcome that supports the hypothesis that resistance training can contribute to reducing dementia risk. These findings support the use of structured resistance training to promote full body health inclusive of physical and cognitive health.
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Fortman, James Alexander. "Computer-Based Cognitive Training for Age-Related Cognitive Decline and Mild Cognitive Impairment." Antioch University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=antioch1353454752.

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Saxton, Judith. "Cognitive and functional decline in Alzheimer's disease." Thesis, University of Reading, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.254512.

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Morrell, Lucy. "Informant reported cognitive decline in older adults." Thesis, Canterbury Christ Church University, 2017. http://create.canterbury.ac.uk/16424/.

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Objectives: Gaining an informant’s perspective on cognitive decline has become an increasingly popular, and recommended practice, in the assessment of dementia. However, concern regarding the accuracy of such reports has been documented. The current study aimed to explore factors that might influence such reports, with a particular focus on informant burden. Design: Using a cross-sectional, single-group design, routinely collected data from 82 patient-informant dyads within a memory assessment service, was analysed. Univariate and multivariate analyses explored associations between informant-reported cognitive decline, demographic characteristics and clinical variables (including burden). Results: None of the demographic characteristics explored were associated with informant-reported cognitive decline. Informant reports were associated with patient cognitive functioning, as assessed by a standardised psychometric measure, and the final outcome of the assessment. Patient affective state and informant-reported burden interacted in influencing informant-reported cognitive decline. Informant-reported burden did not mediate the relationship between informant-reported cognitive decline and patient performance on a standardised psychometric measure. Conclusions: Findings suggest that informant subjective burden predicts informant-reported cognitive decline, and that patient affective state interacts with subjective burden in doing so. Clinical and empirical implications are discussed.
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Li, Xiaoxia. "A Semiparametric Trajectory Model for Cognitive Decline." Diss., North Dakota State University, 2017. http://hdl.handle.net/10365/25922.

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Dementia is a group of diseases that are caused by neurocognitive disorder. It is the second leading cause of death in older adults in the US. People who suffer from dementia experience memory loss and other cognitive or functional decline that is severe enough to interfere with their professional and social performance. In spite of the controversy on accuracy of diagnosis and debate on disclosure of dementia diagnosis results, it is important for patients and their families to know what to expect about the future development of cognitive decline. The course of dementia progression is highly diverse, and the symptoms vary differently from case to case. Amnesia, aphasia, agnosia, and apraxia can exist solely or in combination. The rate of cognitive decline, in the term of Clinical Dementia Rating Score, demonstrated different patterns on an individual level. However, in spite of the variety of symptoms, it is essential to map the cognitive decline to the severity of the impact of the symptoms on daily life. Clinical Dementia Rating SUM score (CDR SUM score) is a comprehensive evaluation based on cognition level. Trajectory modeling can provide a practical tool for physicians to make prognosis and medical trials. Furthermore, trajectory modeling can be a valuable reference for stakeholders to use in reimbursement decisions or policies on caregiving resource allocation. However, there is a gap in the current research to predict the trajectory for cognitive decline. In this research, we studied the typical pattern of CDR SUM scores and predicted a timeline for people with cognitive decline. The innovation and significance of this study is the development of multilevel and semiparametric models, and a simple and straightforward criterion for model evaluation and selection. The model we built showed robustness in both explaining the data and predictions. The study results revealed the factors associated with cognitive decline rate in terms of CDR SUM score, and gave implications on accurate CDR SUM score prediction by individual demographic and clinical profiles. The developed model can also be applied to other longitudinal studies in behavioral science, medical monitoring, and other time series related studies.
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Books on the topic "Cognitive decline"

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Leshner, Alan I., Story Landis, Clare Stroud, and Autumn Downey, eds. Preventing Cognitive Decline and Dementia. Washington, D.C.: National Academies Press, 2017. http://dx.doi.org/10.17226/24782.

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Howard, Fillit, and Butler Robert N. 1927-, eds. Cognitive decline: Strategies for prevention. 2nd ed. London: Greenwich Medical Media, 1997.

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1956-, Brown Don, ed. Dementia and age-related cognitive decline. Seattle, WA: Natural Product Research Consultants, 1997.

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United States. Agency for Healthcare Research and Quality and Duke University Evidence-based Practice Center, eds. Preventing Alzheimer's disease and cognitive decline. Rockville, MD: Agency for Healthcare Research and Quality, 2010.

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The decline and fall of hemispheric specialization. Hillsdale, N.J: Lawrence Erlbaum Associates, 1990.

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Gussekloo, Jacobijn. Determinants of cognitive decline in the oldest old: The Leiden 85-plus study. Leiden: Universiteit Leiden, 2000.

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The decline of intelligence in America: A strategy for national renewal. Westport, Conn: Praeger, 1994.

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Nippak, Pria Melissa Davina. Examination of response latency as an indicator of age-associated cognitive decline in the beagle dog. Ottawa: National Library of Canada, 2002.

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(Editor), Francesco Panza, Vincent Solfrizzi (Editor), and Antonio Capurso (Editor), eds. Diet And Cognitive Decline. Nova Science Publishers, 2005.

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Uysal, Suzan, and David L. Reich. Assessment of Postoperative Cognitive Decline. Edited by David L. Reich, Stephan Mayer, and Suzan Uysal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190280253.003.0007.

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Neurocognitive outcome studies are a potentially rich source of information for evidence-based approaches to neuroprotection. This chapter provides a critical examination of assessment methods for studying postoperative cognitive decline (POCD), with regard to definition of the phenomenon, the role of hypotheses regarding mechanisms and localization of neural injury, and psychometric considerations for the design of POCD assessment protocols. It also describes an approach to conducting clinical neuropsychological assessments outside of research contexts for patients who present with signs or symptoms of POCD when there are no preoperative baseline cognitive test data. The authors propose a set of guidelines for designing, conducting, interpreting, and evaluating cognitive outcome studies in surgical patients and performing clinical POCD assessments.
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Book chapters on the topic "Cognitive decline"

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Polidori, Maria Cristina, Gereon Nelles, Umberto Senin, and Patrizia Mecocci. "Cognitive Decline." In Practical Issues in Geriatrics, 67–80. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-61997-2_7.

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Hedges, Dawson, Thomas J. Farrer, Erin D. Bigler, and Ramona O. Hopkins. "Postoperative Cognitive Decline." In The Brain at Risk, 139–54. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-14260-5_11.

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Xu, Hanzhang, Matthew E. Dupre, and James R. Burke. "Subjective Cognitive Decline." In Encyclopedia of Gerontology and Population Aging, 4798–801. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-22009-9_1136.

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Xu, Hanzhang, Matthew E. Dupre, and James R. Burke. "Subjective Cognitive Decline." In Encyclopedia of Gerontology and Population Aging, 1–4. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-69892-2_1136-1.

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Monsch, Andreas U., Panagiota Mistridis, and Alessandra Thomann. "Postponing Cognitive Decline." In Practical Issues in Geriatrics, 117–27. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-96529-1_13.

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Theisler, Charles. "Dementia/Cognitive Decline." In Adjuvant Medical Care, 90–91. New York: CRC Press, 2022. http://dx.doi.org/10.1201/b22898-103.

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Abrams, David B., J. Rick Turner, Linda C. Baumann, Alyssa Karel, Susan E. Collins, Katie Witkiewitz, Terry Fulmer, et al. "Age-Related Cognitive Decline." In Encyclopedia of Behavioral Medicine, 52. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_100050.

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Lugavere, Max, Alon Seifan, and Richard S. Isaacson. "Prevention of Cognitive Decline." In Handbook on the Neuropsychology of Aging and Dementia, 205–29. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-93497-6_14.

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Gutierrez, Jose, and Richard S. Isaacson. "Prevention of Cognitive Decline." In Handbook on the Neuropsychology of Aging and Dementia, 167–92. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3106-0_12.

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Larroy, Cristina, and Rosa Vera. "Cognitive Decline in Menopause." In Nutrition and Diet in Menopause, 347–57. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-373-2_26.

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Conference papers on the topic "Cognitive decline"

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Souza, João Pedro Ferrari, Wagner Brum, Lucas Hauschild, Lucas Da Ros, Pâmela Lukasewicz Ferreira, Bruna Bellaver, Douglas Leffa, et al. "ASSOCIATION OF VASCULAR RISK AND ALZHEIMER’S DISEASE PATHOLOGY WITH NEURODEGENERATION AND COGNITIVE DECLINE." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda024.

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Background: It is not fully understood how vascular risk factors (VRFs) are associated with Alzheimer’s disease (AD) pathology to promote neurodegeneration and cognitive decline. Objective: Investigate whether VRF burden synergistically interacts with AD pathology to accelerate neurodegeneration and cognitive decline in cognitively unimpaired (CU) individuals. Methods: We assessed 503 CU participants from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database. Individuals were dichotomized as having an elevated VRF burden if ≥ 2 VRFs (V+) and as presenting biological AD if CSF p-tau181 ≥ 24 pg/mL and CSF Aβ1-42 ≤ 976.6 pg/mL [(AT)+]. Neurodegeneration was assessed with plasma neurofilament light (NfL) and cognition with the modified version of the Preclinical Alzheimer’s Cognitive Composite. Results: Linear mixed-effects models demonstrated that an elevated VRF burden interacted with AD pathology to promote higher rates of neurodegeneration (β=5.68, p=.005) and cognitive decline (β=- 0.43, p=.019). Survival analysis demonstrated that only (AT)+V+ individuals had a significantly greater risk of clinical progression to cognitive impairment (adjusted Hazard Ratio=3.5, p <.001). Conclusion: Our results suggest that VRF burden and AD pathology synergistically lead to neurodegeneration and cognitive decline, favoring the onset of cognitive impairment. These findings support that the clinical evaluation of VRF burden might improve the clinical assessment especially of subjects at higher risk for developing cognitive impairment.
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Blackler, Alethea, Doug Mahar, and Vesna Popovic. "Older adults, interface experience and cognitive decline." In the 22nd Conference of the Computer-Human Interaction Special Interest Group of Australia. New York, New York, USA: ACM Press, 2010. http://dx.doi.org/10.1145/1952222.1952257.

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Moya, Manoel Vilela, Mariana Laranjeira Pierotti, and Alyosha Fabiana Rodrigues. "Relationship between hearing loss and cognitive memory decline in an elderly population." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.666.

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Background: The major complaints of the elderly are hearing and memory loss, which have a devastating impact on the communication process. Previous studies have shown that hearing loss is associated with the acceleration of this cognitive decline. Objectives: To analyze the relationship between moderate to moderatelysevere hearing loss and memory deficit in elderly individuals. Design and setting: This is an observational, cross-sectional study realized in seniors of Hearing Care Program at the Taubaté University Hospital, Taubaté - SP/ Brazil. Methods: Data was collected using audiometry, anamnesis, and the cognition test Mini Mental State Examination (MMSE) in 60-75 years old individuals, without knowledge of previous cognitive memory deficit and without the use of hearing aids. Results: Between the 61 seniors interviewed, 68% had moderate degree of deafness and 32% moderately severe degree. Among the normal results in the MMSE, 24% had moderately severe deafness; of those with cognitive impairment without indication of investigation of dementia, 35.7% had moderately severe deafness, and of those with indication of investigation of dementia, 50% had moderately severe deafness. In addition, 23% of the total sample had results in the normal cutoff range, showing the tendency for cognitive decline in this population. Conclusions: these data indicate a progression in the proportion of individuals with a higher degree of hearing loss, the higher the cognitive deficit.
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Almeida, Mariana, Carina Spedo, Ari Pedro Balieiro Júnior, Paulo Caramelli, Sonia Brucki, Benito Damasceno, Ricardo Nitrini, et al. "SUBJECTIVE COGNITIVE DECLINE IN THE BRAZILIAN POPULATION: PRELIMINARY RESULTS OF AN ONLINE STUDY." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda099.

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Background: We observe Subjective Cognitive Decline (SCD) when patients perceive a decline in their cognitive functions, but this decline is not detected in neuropsychological assessments. Few studies have investigated the prevalence of SCD in the Brazilian population. Objective: Analyze the profile of 50+ years Brazilian people regarding SCD through a self-administered online questionnaire Methods: Cross-sectional study, in the online modality. The recruitment of participants took place through email, Facebook, and WhatsApp. Results: We received 1440 responses, mainly from the country’s Southeast region (80.0%). Most of the respondents were female (67.0%), with a mean age of 58.7 (SD=8.5) years, heterosexual (97.3%), skin color referred to as white (84.5%), married (67.6%), post-graduated (51.0%) and working, but not retired (45.5%). About 55.0% reported that their memory has worsened over the past five years and 50.0% of those informed that the worsening of memory worries them. For 38.0% of the respondents, their memory is adequate. Regarding cognitive functions in the last five years, 41.0% claim that they have had problems with attention or concentration, 46.0% that their reasoning has slowed down, and 55% that they have had issues with language. Conclusion: An expressive proportion of the analyzed sample perceived a decline in their cognition at some level.
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Dahy, Flávia, Aline Matos, Thais Romano, Rosa Maria Marcusso, Tatiane Assone, Camila Romano, Augusto Penalva de Oliveira, and Jerusa Smid. "COVID-19 - RELATED COGNITIVE IMPAIRMENT IN PATIENTS FOLLOWED AT A REFERRAL CENTER IN SÃO PAULO, BRAZIL." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda071.

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Background: Central nervous system involvement associated with Coronavirus Disease 2019 (COVID-19) has been reported, including cognitive impairment, even in patients with mild COVID-19. processes. Objective: To assess cognitive decline related to the SARS-CoV-2 infection in patients with neurological disease after COVID-19. Methods: Longitudinal prospective study developed to compare the cognitive performance of patients after COVID-19 based on cognitive complaints. The Addenbrooke´s Cognitive ExaminationRevised (ACE-R), a 100-point test, was applied for investigation, with cut-off score for cognitively normal individuals ≥ 78. Results: Fifty patients were evaluated, 33 women (66%). Thirty-six patients with cognitive complaint (72%), this being the only symptom in 18 (50%), more frequent in women (5:1). Among all patients, the mean score of ACE-R was 80.8 (SD 11) and median of 84. In patients with cognitive complaints, mean of 80.37 (SD 12.2) and median of 84. For the other patients, mean of 81.86 (SD 7.65) and median of 82.5 (p value = 0.9869). Cognitive decline was confirmed in 10/35 (28.57%) of patients with cognitive complaint, and in 4/14 (28.57%) of other patients (exacto de Fisher = 0.8809). Regarding the ACE-R subanalyses, impaired attention and orientation were observed in both groups. Conclusion: Cognitive complaint was not a predictor of cognitive decline, but impairment in attention and orientation were observed in the entire sample.
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Pedrini, Natália Menegassi, Matheus da Silva Calabresi Machado, Matheus Fernando Manzolli Ballestero, and Francisco de Assis Carvalho do Vale. "Demographic characteristics of subjective cognitive decline studies’ samples. A systematic review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.627.

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Background: Subjective cognitive decline (SCD) consists on self-perception of cognition decline without an objective impairment. It has gotten attention from researchers because it may be an early stage of Alzheimer’s disease, before dementia Objectives: This research aimed to determine the characteristics of the SCD studies’ samples across the countries. Methods: It was searched for complete articles from 2014 to 2020 on MEDLINE, PubMed, EMBASE and others, using the keyword “Subjective Cognitive Decline” and its respective translations in both Spanish and Portuguese. Results: Of 3,470 papers, 487 were eligible. The mean age of SCD participants was 71.98 in 2014 to 66.14 in 2020, (mean 66.81) as the number of participants, there were 104 in 2014 and 5233 in 2020 (mean: 1729), and 59% of the participants were women. The mean scholar years were 13.4, in 2014 there were 8 articles and 167 in 2020. Conclusions: The increased number of publications and samples represents the crescent importance of the theme. The decrease in the mean age, possibly demonstrates efforts to an earlier detection of the condition. The majority of women, could represent a prevalence of this gender on the disease, or be related with the fact that woman participate more in scientific studies and also use the health services more than men. The high level of scholarly contrasts with the wrong conception of dementia being related only to poor education, showing that it also affects higher levels of schooling.
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France, Grace, Mark W. Orme, Neil J. Greening, Michael C. Steiner, and Sally J. Singh. "Cognitive decline following an acute exacerbation of COPD (AECOPD)." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.3291.

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Luz, Saturnino, Fasih Haider, Sofia de la Fuente, Davida Fromm, and Brian MacWhinney. "Detecting Cognitive Decline Using Speech Only: The ADReSSo Challenge." In Interspeech 2021. ISCA: ISCA, 2021. http://dx.doi.org/10.21437/interspeech.2021-1220.

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Matic, Aleksandar, and Venet Osmani. "Technologies to monitor cognitive decline - A preliminary case study." In 3d International ICST Conference on Pervasive Computing Technologies for Healthcare. ICST, 2009. http://dx.doi.org/10.4108/icst.pervasivehealth2009.6046.

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Padhee, Swati, Anurag Illendula, Megan Sadler, Valerie L. Shalin, Tanvi Banerjee, Krishnaprasad Thirunarayan, and William L. Romine. "Predicting Early Indicators of Cognitive Decline from Verbal Utterances." In 2020 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2020. http://dx.doi.org/10.1109/bibm49941.2020.9313106.

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Reports on the topic "Cognitive decline"

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Darden, Michael. Cognitive Decline and Dynamic Selection. Cambridge, MA: National Bureau of Economic Research, November 2022. http://dx.doi.org/10.3386/w30679.

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Kane, M.D., Robert L., Mary Butler, Ph.D., M.B.A., and Howard A. Fink, M.D., M.P.H. Interventions To Prevent Age-Related Cognitive Decline, Mild Cognitive Impairment, and Clinical Alzheimer’s-Type Dementia. Agency for Healthcare Research and Quality (AHRQ), 2017. http://dx.doi.org/10.23970/ahrqepccer188.

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Ameriks, John, Andrew Caplin, Minjoon Lee, Matthew Shapiro, and Christopher Tonetti. Cognitive Decline, Limited Awareness, Imperfect Agency, and Financial Well-being. Cambridge, MA: National Bureau of Economic Research, January 2022. http://dx.doi.org/10.3386/w29634.

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Fillipin, Federico, Pamela Seron, and Ruvistay Gutierrez-Arias. Effectiveness of antihypertensive drugs to prevent cognitive decline, mild cognitive impairment, and dementia. An overview of systematic reviews. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2022. http://dx.doi.org/10.37766/inplasy2022.12.0057.

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Review question / Objective: To determine effectiveness of antihypertensive drugs to prevent different dementia subtypes such as Alzheimer’s disease and vascular dementia. Condition being studied: Dementia is a global health burden, with the number of affected individuals increasing. A recent meta-analysis reported that the prevalence of all-type dementia was 697 per 10,000 people and the prevalence of Alzheimer’s disease was 324 per 10,000 people. The SHEP and SYST-EUR were the two first randomized controlled trials to show that hypertension treatment reduces dementia risk.
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Fremouw, Thane, Maxwell Hennings, Christy Fessler, Hawk Cambron, Teresa Collins, and Moriah Greer. Chemotherapy, Neurotoxicity, and Cognitive Decline: Developing a Mouse Model and Potential Interventions. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada568167.

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Fremouw, Thane. Chemotheraphy, Neurotoxicity, and Cognitive Decline: Developing a Mouse Model and Potential Interventions. Fort Belvoir, VA: Defense Technical Information Center, September 2011. http://dx.doi.org/10.21236/ada555413.

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Hu, XinYi, JingXuan Hao, and HangYue Wang. Improvement of Environmental enrichment on Cognitive Functions in Patients and animals : A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2022. http://dx.doi.org/10.37766/inplasy2022.12.0014.

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Review question / Objective: To study the relationship between environmental enrichment and cognitive function through a meta-analysis of the literature, analyze its effects on the improvement of cognitive function in patients and animals, and evaluate the effects of different environmental enrichment measures on cognitive function improvement. Condition being studied: Cognitive decline refers to an individual's memory, language, reasoning and other aspects of cognitive function showing obvious, measurable decline or abnormal. The causes of cognitive decline are various, including neurodegeneration, cerebrovascular disease, infection, trauma, and depression. Alzheimer's disease and stroke are the most common.
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Hudomiet, Péter, Michael Hurd, Susann Rohwedder, and Robert Willis. The Effect of Physical and Cognitive Decline at Older Ages on Job Mismatch and Retirement. Cambridge, MA: National Bureau of Economic Research, November 2018. http://dx.doi.org/10.3386/w25229.

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Mehegan, Laura, and Chuck Rainville. Perceptions of Dementia: 2022 AARP Focus Groups and In-Depth Interviews on Dementia and Cognitive Decline. Washington, DC: AARP Research, January 2023. http://dx.doi.org/10.26419/res.00471.007.

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Singh, Ruchi, Akhiya Nail, and Nirendra Kumar Rai. Effectiveness of Vitamin B12 Supplementation on cognitive, motor & mood instability of Parkinson’s disease patients on levodopa treatment :A Systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2023. http://dx.doi.org/10.37766/inplasy2023.2.0066.

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Review question / Objective: The treatment of choice for patients of Parkinson's disease is levodopa. However, levodopa has been suggested to decrease Vit B12 level in these patients. Thus, the research question for this systematic review is whether vit B 12 supplementation in Parkinson's disease(PD) patients on treatment with levodopa improves vit B12 level effecting the Cognition, Motor functions and Mood instability among them in comparison to PD patients on levodopa treatment who are not supplemented with Vit B12. Condition being studied: Parkinson disease is the progressive degeneration of dopaminergic neurons present within the substantia nigra that can lead to altered movements along with the prevalence of cognitive and mood instability as a result of dopamine(neurotransmitter) deficiency. The most effective treatment for the Parkinson's disease is the administration of levodopa, a dopamine precursor . Long term treatment with levodopa causes an increase in homocysteine levels and tissue deficiency of vitamin B12 and folate may occur. Vitamin B12 supplementation is administered as after management regime, in Parkinson patient on levodopa treatment . This study aims to conduct a systematic review, of studies , randomized control trials investigating the ability of vitamin B12 supplementation to enhances the recovery/reduce the decline, if any, of the symptoms of cognitive, motor, mood impairments associated with Parkinson's disease patient on levodopa treatment.
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