There is increasing recognition of social health being protective against disease, including age-related cognitive decline and dementia. Many concepts around social health, reserve and connectedness ...are imprecise and without agreed definitions. The mechanisms by which social health is protective are not well understood.
Several observational studies suggest that social participation and connectedness are protective against cognitive decline whereas loneliness is a risk factor for dementia. The possible mechanisms include effects on inflammatory process and immune function, reduced vascular disease risk, improved health behaviours, lower risk of depression, and increased cognitive reserve through cognitive stimulation and physical activity. Social networks have been shown to modify the relationship between Alzheimer's disease and cognitive impairment. The relationship of social networks is, however, reciprocal, with dementia leading to social loss, which in turn worsens cognitive decline. Social reserve is conceptualized as both brain processes underlying the ability and predisposition to form meaningful social ties, and their instantiation as an environmental resource in high-quality social networks.
Consistent definitions of social health-related terms will lead to better understanding of their determinants so that tailored interventions can be developed to increase social reserve and improve social health of an individual.
Social cognition broadly refers to the processing of social information in the brain that underlies abilities such as the detection of others' emotions and responding appropriately to these emotions. ...Social cognitive skills are critical for successful communication and, consequently, mental health and wellbeing. Disturbances of social cognition are early and salient features of many neuropsychiatric, neurodevelopmental and neurodegenerative disorders, and often occur after acute brain injury. Its assessment in the clinic is, therefore, of paramount importance. Indeed, the most recent edition of the American Psychiatric Association's Diagnostic and Statistical Manual for Mental Disorders (DSM-5) introduced social cognition as one of six core components of neurocognitive function, alongside memory and executive control. Failures of social cognition most often present as poor theory of mind, reduced affective empathy, impaired social perception or abnormal social behaviour. Standard neuropsychological assessments lack the precision and sensitivity needed to adequately inform treatment of these failures. In this Review, we present appropriate methods of assessment for each of the four domains, using an example disorder to illustrate the value of these approaches. We discuss the clinical applications of testing for social cognitive function, and finally suggest a five-step algorithm for the evaluation and treatment of impairments, providing quantitative evidence to guide the selection of social cognitive measures in clinical practice.
The AT(N) research framework was introduced in 2018 to define Alzheimer's disease as a biological entity. It is recognized that Alzheimer's disease lesions rarely occur in isolation in older brains, ...with cerebrovascular disease (CVD) being a common comorbidity. To fully characterize the disorder of dementia, the AT(N) framework needs to be extended with biomarkers for other disorders. The present review examines some of the requirements for adding a 'V' to the AT(N), and examines the currently available biomarkers as definitive markers of CVD.
Neuroimaging biomarkers of CVD have received the greatest attention, with rapid advances in MRI techniques showing the greatest promise. Challenges remain in standardization of techniques, validation of some of the results and assessing total CVD burden from diverse lesion types. Retinal imaging shows promise as a window to cerebral vasculature. Biochemical markers are advancing rapidly, but their specificity for CVD is not established.
Biomarkers of CVD have seen rapid advances but further validation and determination of their specificity are needed before they can be reliably used to delineate a V in the AT(N) framework as definitive indicators of significant CVD.
Mild cognitive impairment (MCI) increases dementia risk with no pharmacologic treatment available.
The Study of Mental and Resistance Training was a randomized, double-blind, double-sham controlled ...trial of adults with MCI. Participants were randomized to 2 supervised interventions: active or sham physical training (high intensity progressive resistance training vs seated calisthenics) plus active or sham cognitive training (computerized, multidomain cognitive training vs watching videos/quizzes), 2-3 days/week for 6 months with 18-month follow-up. Primary outcomes were global cognitive function (Alzheimer's Disease Assessment Scale-cognitive subscale; ADAS-Cog) and functional independence (Bayer Activities of Daily Living). Secondary outcomes included executive function, memory, and speed/attention tests, and cognitive domain scores.
One hundred adults with MCI 70.1 (6.7) years; 68% women were enrolled and analyzed. Resistance training significantly improved the primary outcome ADAS-Cog; relative effect size (95% confidence interval) -0.33 (-0.73, 0.06); P < .05 at 6 months and executive function (Wechsler Adult Intelligence Scale Matrices; P = .016) across 18 months. Normal ADAS-Cog scores occurred in 48% (24/49) after resistance training vs 27% (14/51) without resistance training P < .03; odds ratio (95% confidence interval) 3.50 (1.18, 10.48). Cognitive training only attenuated decline in Memory Domain at 6 months (P < .02). Resistance training 18-month benefit was 74% higher (P = .02) for Executive Domain compared with combined training z-score change = 0.42 (0.22, 0.63) resistance training vs 0.11 (-0.60, 0.28) combined and 48% higher (P < .04) for Global Domain z-score change = .0.45 (0.29, 0.61) resistance training vs 0.23 (0.10, 0.36) combined.
Resistance training significantly improved global cognitive function, with maintenance of executive and global benefits over 18 months.
Type 2 diabetes (diabetes) is characterized by accelerated cognitive decline and higher dementia risk. Controversy exists regarding the impact of metformin, which is associated with both increased ...and decreased dementia rates. The objective of this study was to determine the association of metformin use with incident dementia and cognitive decline over 6 years in participants with diabetes compared with those not receiving metformin and those without diabetes.
A prospective observational study was conducted of
= 1,037 community-dwelling older participants without dementia aged 70-90 years at baseline (the Sydney Memory and Ageing Study). Exclusion criteria were dementia, major neurological or psychiatric disease, or progressive malignancy. Neuropsychological testing measured cognitive function every 2 years; a battery of tests measured executive function, memory, attention/speed, language, and visuospatial function individually. These were used to determine the measure of global cognition. Incident dementia was ascertained by a multidisciplinary panel. Total brain, hippocampal, and parahippocampal volumes were measured by MRI at baseline and 2 years (
= 526). Data were analyzed by linear mixed modeling, including the covariates of age, sex, education, BMI, heart disease, hypertension, stroke, smoking, and apolipoprotein Eε4 carriage.
Of
= 1,037, 123 had diabetes; 67 received metformin (DM+MF) and were demographically similar to those who did not (DM-noMF) and participants without diabetes (no-DM). DM+MF had significantly slower global cognition and executive function decline compared with DM-noMF. Incident dementia was significantly higher in DM-noMF compared with DM+MF (odds ratio 5.29 95% CI 1.17-23.88;
= 0.05).
Older people with diabetes receiving metformin have slower cognitive decline and lower dementia risk. Large randomized studies in people with and without diabetes will determine whether these associations can be attributed to metformin.
Abstract The brain is highly enriched in lipids, and an intensive study of these lipids may be informative, not only of normal brain function but also of changes with age and in disease. In recent ...years, the development of highly sensitive mass spectrometry platforms and other high-throughput technologies has enabled the discovery of complex changes in the entire lipidome. This lipidomics approach promises to be a particularly useful tool for identifying diagnostic biomarkers for early detection of age-related neurodegenerative disease, such as Alzheimer's disease (AD), which has till recently been limited to protein- and gene-centric approaches. This review highlights known lipid changes affecting the AD brain and presents an update on the progress of lipid biomarker research in AD. Important considerations for designing large-scale lipidomics experiments are discussed to help standardize findings across different laboratories, as well as challenges associated with moving toward clinical application.
•Relationships examined among cortical gyrification, volumes & thickness in mid-life.•Positive gyrification–volume & negative gyrification–thickness relationships found.•Positive ...gyrification–cognition relationships found in frontal cortex.•Small sex differences in cortical gyrification controlling for cortex volumes.
Across species, greater cortical gyrification, or folding of the cortex, has been shown to be associated with higher cognitive abilities and is thought to reflect an evolutionary process aimed at maximizing the number of cerebral computational units while minimizing the energy and communication costs of larger brains. Relatively little is known about the significance of individual variation in gyrification in humans and how it relates to other aspects of cerebral structure and function. In the current study, we examined relationships between cortical gyrification and (i) cortical volume, (ii) cortical thickness, and (iii) executive functions. Participants were middle-aged healthy adults (44–48 years old, n=396) in a community-based sample. T1-weighted 3D structural magnetic resonance imaging scans were acquired in a Fast Field Echo sequence. Cortical gyrification, volume, and thickness were measured through the semi-automated software FreeSurfer. Results showed that cortical gyrification was strongly and positively related to cortical volume, but was negatively related to cortical thickness in many regions of the cortex. In addition, frontal gyrification was positively related to performance in working memory and mental flexibility tasks. These results support the view that greater cortical gyrification is related both to bigger brain volumes and better cognitive function, but not to greater cortical thickness. The results provide evidence of functional relevance of cortical gyrification development, and show that it can be a useful index to investigate structure–cognition relationships.
PDF
