scholarly journals Cognitive Trajectories and Dementia Risk: A Comparison of Two Cognitive Reserve Measures

2021 ◽  
Vol 13 ◽  
Author(s):  
Federico Gallo ◽  
Grégoria Kalpouzos ◽  
Erika J. Laukka ◽  
Rui Wang ◽  
Chengxuan Qiu ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Cognitive Reserve ◽  
Cognitive Change ◽  
National Study ◽  
Residual Variance ◽  
Dementia Risk ◽  
Dementia Incidence ◽  
Integrity Index ◽  
The Impact ◽  
The Brain

Background and ObjectivesCognitive reserve (CR) is meant to account for the mismatch between brain damage and cognitive decline or dementia. Generally, CR has been operationalized using proxy variables indicating exposure to enriching activities (activity-based CR). An alternative approach defines CR as residual variance in cognition, not explained by the brain status (residual-based CR). The aim of this study is to compare activity-based and residual-based CR measures in their association with cognitive trajectories and dementia. Furthermore, we seek to examine if the two measures modify the impact of brain integrity on cognitive trajectories and if they predict dementia incidence independent of brain status.MethodsWe used data on 430 older adults aged 60+ from the Swedish National Study on Aging and Care in Kungsholmen, followed for 12 years. Residual-based reserve was computed from a regression predicting episodic memory with a brain-integrity index incorporating six structural neuroimaging markers (white-matter hyperintensities volume, whole-brain gray matter volume, hippocampal volume, lateral ventricular volume, lacunes, and perivascular spaces), age, and sex. Activity-based reserve incorporated education, work complexity, social network, and leisure activities. Cognition was assessed with a composite of perceptual speed, semantic memory, letter-, and category fluency. Dementia was clinically diagnosed in accordance with DSM-IV criteria. Linear mixed models were used for cognitive change analyses. Interactions tested if reserve measures modified the association between brain-integrity and cognitive change. Cox proportional hazard models, adjusted for brain-integrity index, assessed dementia risk.ResultsBoth reserve measures were associated with cognitive trajectories [β × time (top tertile, ref.: bottom tertile) = 0.013; 95% CI: –0.126, –0.004 (residual-based) and 0.011; 95% CI: –0.001, 0.024, (activity-based)]. Residual-based, but not activity-based reserve mitigated the impact of brain integrity on cognitive decline [β (top tertile × time × brain integrity) = –0.021; 95% CI: –0.043, 0.001] and predicted 12-year dementia incidence, after accounting for the brain-integrity status [HR (top tertile) = 0.23; 95% CI: 0.09, 0.58].InterpretationThe operationalization of reserve based on residual cognitive performance may represent a more direct measure of CR than an activity-based approach. Ultimately, the two models of CR serve largely different aims. Accounting for brain integrity is essential in any model of reserve.

Comparison of Education and Episodic Memory as Modifiers of Brain Atrophy Effects on Cognitive Decline: Implications for Measuring Cognitive Reserve

2021 ◽  
pp. 1-11
Author(s):  
Dan Mungas ◽  
Evan Fletcher ◽  
Brandon E. Gavett ◽  
Keith Widaman ◽  
Laura B. Zahodne ◽  
...  
Keyword(s):  
Episodic Memory ◽  
Cognitive Decline ◽  
Gray Matter ◽  
Cognitive Abilities ◽  
Cognitive Reserve ◽  
Cognitive Change ◽  
Interactive Effects ◽  
Neural Basis ◽  
Atrophy Rate ◽  
The Impact

Abstract Objective: This study compared the level of education and tests from multiple cognitive domains as proxies for cognitive reserve. Method: The participants were educationally, ethnically, and cognitively diverse older adults enrolled in a longitudinal aging study. We examined independent and interactive effects of education, baseline cognitive scores, and MRI measures of cortical gray matter change on longitudinal cognitive change. Results: Baseline episodic memory was related to cognitive decline independent of brain and demographic variables and moderated (weakened) the impact of gray matter change. Education moderated (strengthened) the gray matter change effect. Non-memory cognitive measures did not incrementally explain cognitive decline or moderate gray matter change effects. Conclusions: Episodic memory showed strong construct validity as a measure of cognitive reserve. Education effects on cognitive decline were dependent upon the rate of atrophy, indicating education effectively measures cognitive reserve only when atrophy rate is low. Results indicate that episodic memory has clinical utility as a predictor of future cognitive decline and better represents the neural basis of cognitive reserve than other cognitive abilities or static proxies like education.

scholarly journals Spousal Loss and Cognitive Functioning: Do Pre-Loss Marital Quality and Gender Matter?

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 366-366
Author(s):  
Joohong Min ◽  
Jieun Song
Keyword(s):  
Cognitive Decline ◽  
Cognitive Functioning ◽  
Marital Quality ◽  
The United States ◽  
Cognitive Change ◽  
Life Transitions ◽  
Cognitive Changes ◽  
Spousal Loss ◽  
And Gender ◽  
The Impact

Abstract Prior research has found that the risk of cognitive decline increases after the death of a spouse. In general, the impact of life transitions is contingent on contextual factors such as socio-demographic characteristics or relationship quality. However, there is limited research on how marital quality before spousal loss and gender influence the association between spousal loss and cognitive change. The current study examines the effects of spousal loss on change in cognitive functioning as well as the moderating effects of pre-loss marital quality and gender. Data from two waves of the Midlife in the United States (MIDUS) study were analyzed (MIDUS2: 2004-05, MIDUS3: 2013-14). The analytic sample consists of two groups: (1) 179 bereaved adults who were age 54 or older at MIDUS2 (M = 65.2, SD = 9.5) and whose spouses died between MIDUS2 and MIDUS3, and (2) 179 non-bereaved adults, matched with the bereaved group on age and gender, who did not experience spousal loss between the two waves. Cognitive function was assessed via BTACT (Brief Telephone Adult Cognition Test) at both waves. Regression results show that both pre-loss marital quality and gender significantly moderate the association between spousal loss and change in cognitive functioning. Specifically, relative to their counterparts, men and those who reported better marital relationships prior to spousal death had a greater risk of cognitive decline after a spouse’s death. The findings suggest the significance of pre-loss marital quality and gender for cognitive changes in widowhood and have implications for the development of efficient interventions

scholarly journals Dementia risk communication. A user manual for Brain Health Services—part 3 of 6

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Leonie N. C. Visser ◽  
Carolina Minguillon ◽  
Gonzalo Sánchez-Benavides ◽  
Marc Abramowicz ◽  
Daniele Altomare ◽  
...  
Keyword(s):  
Health Services ◽  
Risk Communication ◽  
Disease Status ◽  
Prevention Programs ◽  
Brain Health ◽  
Individual Level ◽  
Risk Profiling ◽  
Dementia Risk ◽  
Dementia Incidence ◽  
The Impact

AbstractGrowing evidence suggests dementia incidence can be reduced through prevention programs targeting risk factors. To accelerate the implementation of such prevention programs, a new generation of brain health services (BHS) is envisioned, involving risk profiling, risk communication, risk reduction, and cognitive enhancement. The purpose of risk communication is to enable individuals at risk to make informed decisions and take action to protect themselves and is thus a crucial step in tailored prevention strategies of the dementia incidence. However, communicating about dementia risk is complex and challenging.In this paper, we provide an overview of (i) perspectives on communicating dementia risk from an ethical, clinical, and societal viewpoint; (ii) insights gained from memory clinical practice; (iii) available evidence on the impact of disclosing APOE and Alzheimer’s disease biomarker test results gathered from clinical trials and observational studies; (iv) the value of established registries in light of BHS; and (v) practical recommendations regarding effective strategies for communicating about dementia risk.In addition, we identify challenges, i.e., the current lack of evidence on what to tell on an individual level—the actual risk—and on how to optimally communicate about dementia risk, especially concerning worried yet cognitively unimpaired individuals. Ideally, dementia risk communication strategies should maximize the desired impact of risk information on individuals’ understanding of their health/disease status and risk perception and minimize potential harms. More research is thus warranted on the impact of dementia risk communication, to (1) evaluate the merits of different approaches to risk communication on outcomes in the cognitive, affective and behavioral domains, (2) develop an evidence-based, harmonized dementia risk communication protocol, and (3) develop e-tools to support and promote adherence to this protocol in BHSs.Based on the research reviewed, we recommend that dementia risk communication should be precise; include the use of absolute risks, visual displays, and time frames; based on a process of shared decision-making; and address the inherent uncertainty that comes with any probability.

Cognitive reserve moderates the impact of subcortical gray matter atrophy on neuropsychological status in multiple sclerosis

2015 ◽  
Vol 22 (1) ◽  
pp. 36-42 ◽  
Author(s):  
Claire M Modica ◽  
Niels Bergsland ◽  
Michael G Dwyer ◽  
Deepa P Ramasamy ◽  
Ellen Carl ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Cognitive Decline ◽  
Cognitive Processing ◽  
Gray Matter ◽  
Cognitive Reserve ◽  
Cognitive Outcome ◽  
Brain Reserve ◽  
The Impact ◽  
Normal Controls

Background: Cognitive decline is characterized in multiple sclerosis (MS), but the rate and severity vary. The reserve hypothesis proposes that baseline neurological differences impact cognitive outcome in neurodegenerative disease. Objective: To elucidate how brain reserve and cognitive reserve influence subcortical gray matter (SCGM) atrophy and cognitive decline in MS over 3 years. Methods: Seventy-one MS patients and 23 normal controls underwent magnetic resonance imaging and cognitive assessment at baseline and 3-year follow-up. The influence of reserve on cognitive processing speed (CPS) and memory was examined. Results: SCGM volume and cognitive scores were lower in MS than normal controls ( P⩽0.001). Accounting for baseline, comparison of follow-up means yielded a difference between groups in SCGM volume ( P<0.001) but not cognition (NS). Cognitive reserve ( P=0.005), but not brain reserve, contributed to CPS, with only low cognitive reserve MS subjects showing decline in CPS ( P=0.029). SCGM change predicted CPS outcome in MS with low cognitive reserve ( P=0.002) but not high cognitive reserve. There were no effects in the domain of memory. Conclusions: SCGM atrophy occurs in normal controls, but significantly more so in MS. While CPS did not change in normal controls, low cognitive reserve was associated with CPS decline in MS. High cognitive reserve protect MS patients from cognitive decline related to SCGM atrophy.

The Impact of Amyloid-β or Tau on Cognitive Change in the Presence of Severe Cerebrovascular Disease

2020 ◽  
Vol 78 (2) ◽  
pp. 573-585
Author(s):  
Hyemin Jang ◽  
Hee Jin Kim ◽  
Yeong Sim Choe ◽  
Soo-Jong Kim ◽  
Seongbeom Park ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Cognitive Decline ◽  
Interaction Effect ◽  
Significant Interaction ◽  
Amyloid Β ◽  
Cognitive Change ◽  
Significant Interaction Effect ◽  
The Impact

Background: As Alzheimer’s disease (AD) and cerebral small vessel disease (CSVD) commonly coexist, the interaction between two has been of the considerable interest. Objective: We determined whether the association of Aβ and tau with cognitive decline differs by the presence of significant CSVD. Methods: We included 60 subcortical vascular cognitive impairment (SVCI) from Samsung Medical Center and 82 Alzheimer’s disease-related cognitive impairment (ADCI) from ADNI, who underwent Aβ (florbetaben or florbetapir) and tau (flortaucipir, FTP) PET imaging. They were retrospectively assessed for 5.0±3.9 and 5.6±1.9 years with Clinical Dementia Rating-sum of boxes (CDR-SB)/Mini-Mental State Examination (MMSE). Mixed effects models were used to investigate the interaction between Aβ/tau and group on CDR-SB/MMSE changes. Results: The frequency of Aβ positivity (45% versus 54.9%, p = 0.556) and mean global FTP SUVR (1.17±0.21 versus 1.16±0.17, p = 0.702) were not different between the two groups. We found a significant interaction effect of Aβ positivity and SVCI group on CDR-SB increase/MMSE decrease (p = 0.013/p < 0.001), and a significant interaction effect of global FTP uptake and SVCI group on CDR-SB increase/MMSE decrease (p < 0.001 and p = 0.030). Finally, the interaction effects of regional tau and group were prominent in the Braak III/IV (p = 0.001) and V/VI (p = 0.003) not in Braak I/II region (p = 0.398). Conclusion: The association between Aβ/tau and cognitive decline is stronger in SVCI than in ADCI. Therefore, our findings suggested that Aβ positivity or tau burden (particularly in the Braak III/IV or V/VI regions) and CSVD might synergistically affect cognitive decline.

scholarly journals Association between plasma phospho-tau181 and cognitive change from age 73 to 82: Lothian Birth Cohort 1936

2021 ◽  
Author(s):  
Tyler S Saunders ◽  
Amanda Heslegrave ◽  
Declan King ◽  
Sarah Harris ◽  
Craig W Ritchie ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Cognitive Change ◽  
Synaptic Function ◽  
Blood Biomarker ◽  
Array Tomography ◽  
Age Related ◽  
Lothian Birth Cohort ◽  
Synapse Degeneration ◽  
Age Related Cognitive Decline ◽  
The Brain

INTRODUCTION: Plasma phospho-tau 181 (p-tau181) is a promising blood biomarker for Alzheimer's disease. However, its predictive validity for age-related cognitive decline without dementia remains unclear. Several forms of p-tau have been shown to contribute to synapse degeneration, but it is unknown whether p-tau181 is present in synapses. Here, we tested whether plasma p-tau181predicts cognitive decline and whether it is present in synapses in human brain. METHODS: General cognitive ability and plasma p-tau181 concentration were measured in 195 participants at ages 72 and 82. Levels of p-tau181 in total homogenate and synaptic fractions were compared with western blot (n=10-12 per group), and synaptic localisation was examined using array tomography. RESULTS: Elevated baseline plasma p-tau181 and increasing p-tau181 over time predicted steeper general cognitive decline. We observe p-tau181 in neurites, presynapses, and post-synapses in the brain. DISCUSSION: Baseline and subsequent change in plasma p-tau181 may represent rare biomarkers of differences in cognitive ageing across the 8th decade of life and may play a role in synaptic function in the brain.

Lowering dementia risk and slowing progression of disease: the role of cognitive reserve and cognitive training

2020 ◽  
pp. 1-2 ◽  
Author(s):  
Jeffrey F. Scherrer ◽  
John E. Morley
Keyword(s):  
Educational Level ◽  
Cognitive Reserve ◽  
Leisure Activities ◽  
Inverse Correlation ◽  
Data Set ◽  
Dementia Risk ◽  
Dementia Incidence ◽  
Early Dementia ◽  
Progression Of Disease

Summary Almeida-Meza et al found an inverse correlation between cognitive reserve (associated with educational level, complexity of occupations and leisure activities) and dementia incidence. We suggest clarifying studies using their data-set and consider what can be done to modify socioeconomic inequalities that affect cognitive reserve or to slow early dementia.

scholarly journals Hypertension and the Brain: A Risk Factor for More Than Heart Disease

2016 ◽  
Vol 42 (3-4) ◽  
pp. 255-262 ◽  
Author(s):  
Anja Meissner
Keyword(s):  
Risk Factor ◽  
Cognitive Impairment ◽  
Cognitive Decline ◽  
Small Vessel Disease ◽  
Current Knowledge ◽  
White Matter Lesions ◽  
Cerebrovascular Complications ◽  
Cerebrovascular Function ◽  
The Impact ◽  
The Brain

Background: Cerebral small vessel disease (cSVD), a common risk factor for cognitive impairment, involves unspecific arteriopathy characterized by hypertrophy and endothelial dysfunction that alter cerebrovascular function and auto-regulation of cerebral blood flow (CBF). Microbleedings, subcortical lacunar infarctions and diffuse areas of white matter lesions resulting from vascular injury are associated with reduced cognitive function mostly characterized by difficulties in learning and retention, attention deficits, gait disorders or depression. In recent years, it has become evident that vascular risk factors contribute to the development of cSVD and associated vascular cognitive impairment (VCI). Among them, hypertension emerged as such a major modifiable risk factor since the brain presents an early target for organ damage due to changes in blood pressure (BP). Subsequently both high and, especially in the elderly, low BP have been linked to cognitive decline, which initiated controversial discussions about BP control as a potential therapeutic strategy to achieve optimal brain perfusion and thus, reduce the occurrence of cSVD and cognitive dysfunction. Yet, recent randomized controlled trials examined the impact of anti-hypertensive therapy on cognitive performance with conflicting results. Summary: In light of the current knowledge, it becomes apparent that there is an urgent need to understand the mechanisms underlying hypertension-induced cerebrovascular complications in order to identify effective therapeutic targets to prevent and most importantly also reverse cognitive decline mediated through hypertension. Key Message: This review summarizes the current knowledge of cSVD pathogenesis as well as possible links to hypertension-mediated cerebrovascular complications. By pointing out knowledge gaps, it aims to spur future studies in search of specific targets helping to prevent therapy failures and decelerate the rapidly progressing neuro-degeneration of patients suffering from cerebrovascular diseases emanating from hypertension.

scholarly journals 548 - Cognitive aging and cognitive reserve

2021 ◽  
Vol 33 (S1) ◽  
pp. 90-91
Author(s):  
Alena Sidenkova
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Cognitive Decline ◽  
Cognitive Reserve ◽  
Brain Activity ◽  
Clinical Manifestations ◽  
Cognitive Disorders ◽  
Moderate Cognitive Impairment ◽  
The Brain

IntroductionThe aging processes are accelerating in all regions of the world. The involvement of older people in production and social processes determines the need to maintain a high level of social and psychological adaptation, despite the progressive pathology of the brain caused by its aging. This increases the relevance of research related to the study of biological reserves of the brain and psychological and social mechanisms of human adaptation in late adulthood. The risk of developing cognitive disorders is not fatal. According to some observations, even in the hippocampal type of UKR, despite the content of amyloid in the brain, the functional and social activity of the elderly remains high. Prospective studies show that people with high cognitive reserve have a lower risk of developing dementia. Cognitive reserve is the brain’s resistance to damage. Cognitive reserve is the ability of the brain to cope with the consequences of damage caused by external influences, brain stroke, chronic brain ischemia, neurodegenerative diseases, and age-related changes. Cognitive reserve is the brain’s ability to functionally compensate for and minimize clinical manifestations of cognitive impairment. The mechanisms of cognitive reserve in normal and Alzheimer’s disease are different. In healthy older adults, a higher cognitive reserve correlates with larger brain sizes and effective strategies for performing cognitive tasks. In the early stages of Alzheimer’s disease and Alzheimer’s disease, the size of the brain decreases. But high brain activity helps preserve cognitive resources. Excessive brain activity in dementia is a compensatory mechanism. This is confirmed by the results of functional magnetic resonance imaging of the brain. Of course, the degree of brain atrophy is a predisposing factor for dementia, but it is not a mandatory factor for cognitive decline. So, the symptoms of dementia do not appear until you have crossed the critical border of damage to the brain substance. Progressive brain atrophy underlies the clinical manifestations of dementia in neurodegenerative diseases, but the correlation between the degree of brain damage and cognitive impairment is not linear.Research materials and methodsAn observational 10-year longitudinal study was conducted. In 2006, moderate cognitive impairment was found in 66 patients. The group of patients included 49 women and 49 men. Their average age in 2006 was 59.3±5.2 years. In 2006, the severity of cognitive decline was 26.2±1.9 points on the MMSE scale. This corresponds to indicators of moderate cognitive impairment. Research methods: clinical and psychopathological, psychometric, statistical. Questionnaire “Loss and acquisition of personal resources” (N. Vodopyanova, M. Stein), MMSE scale.Research resultIn 2006, amyloid was detected in the spinal fluid of all patients selected for the study group. If a patient developed dementia, they were given specific therapy. The dynamics of cognitive functions in patients was different. Mild dementia was formed in 53% of patients. Moderate dementia was formed in 10.6% of patients. Moderate cognitive impairment (pre-dementia) persisted in 36.4% of patients. Hereditary burden of dementia in patients with moderate dementia was detected 2 times more often. Back in 2006, we identified the leading sensory systems of patients. The master sensor system determines the modality of the main information flow. This is the most important part of the information that a person interacts with. This is the basis of interaction with reality. This is the basis of cognitive functions. Correlations of age-specific lesions of the corresponding sensory systems with the severity of cognitive decline were found in patients with the corresponding sensory modality (Spearman’s Correlation Coefficient-r, p<0.05): presbyacoussis – auditory r=0.667, presbyopia-visual r=0.705. The influence of psychosocial factors on the condition of patients was studied. In dementia, significant history of psychotrauma was found in 35.7%. Moderate stress was detected in the group of patients with moderate cognitive impairment in 33.3%. Moderate stress was detected in the group of patients with dementia in 83.3%. Stress of loss of life meaning was detected more often in patients with dementia 76.7%. It is important not only what stresses a person endures, but how they can cope with them. Dementia patients were statistically more likely to have unproductive coping strategies that did not help them cope adequately with stress.ConclusionsThe concept of cognitive reserve suggests possible causes of heterogeneity in the dynamics of cognitive decline in the initial stages of atrophic-degenerative brain diseases: biological causes and psychosocial causes. The concept of cognitive reserve helps to study and develop individual programs for the prevention of severe cognitive disorders.

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