https://www.sfs.uni-tuebingen.de/~hbaayen/publications/baayenDavidsonBates.pdf

Mixed-effects modeling with crossed random effects for subjects and items

During the past 20 years there has been a dramatic increase in societal interest in preventing disability and death in the United States by changing individual behaviors linked to the risk of contracting chronic diseases. This renewed interest in health promotion and disease prevention has not been without its critics. Some critics have accused proponents of life-style interventions of promoting a victim-blaming ideology by neglecting the importance of social influences on health and disease. This article proposes an ecological model for health promotion which focuses attention on both individual and social environmental factors as targets for health promotion interventions. It addresses the importance of interventions directed at changing interpersonal, organizational, community, and public policy, factors which support and maintain unhealthy behaviors. The model assumes that appropriate changes in the social environment will produce changes in individuals, and that the support of individuals in the population is essential for implementing environmental changes.

An Ecological Perspective on Health Promotion Programs

The hippocampus shrinks in late adulthood, leading to impaired memory and increased risk for dementia. Hippocampal and medial temporal lobe volumes are larger in higher-fit adults, and physical activity training increases hippocampal perfusion, but the extent to which aerobic exercise training can modify hippocampal volume in late adulthood remains unknown. Here we show, in a randomized controlled trial with 120 older adults, that aerobic exercise training increases the size of the anterior hippocampus, leading to improvements in spatial memory. Exercise training increased hippocampal volume by 2%, effectively reversing age-related loss in volume by 1 to 2 y. We also demonstrate that increased hippocampal volume is associated with greater serum levels of BDNF, a mediator of neurogenesis in the dentate gyrus. Hippocampal volume declined in the control group, but higher preintervention fitness partially attenuated the decline, suggesting that fitness protects against volume loss. Caudate nucleus and thalamus volumes were unaffected by the intervention. These theoretically important findings indicate that aerobic exercise training is effective at reversing hippocampal volume loss in late adulthood, which is accompanied by improved memory function.

https://www.pnas.org/content/pnas/108/7/3017.full.pdf

Exercise training increases size of hippocampus and improves memory

https://journals.plos.org/plosmedicine/article/file?id=10.1371/journal.pmed.0040297&type=printable

Strengthening the Reporting of Observational Studies in Epidemiology (STROBE): Explanation and elaboration

Components of heart rate variability have attracted considerable attention in psychology and medicine and have become important dependent measures in psychophysiology and behavioral medicine. Quantification and interpretation of heart rate variability, however, remain complex issues and are fraught with pitfalls. The present report (a) examines the physiological origins and mechanisms of heart rate variability, (b) considers quantitative approaches to measurement, and (c) highlights important caveats in the interpretation of heart rate variability. Summary guidelines for research in this area are outlined, and suggestions and prospects for future developments are considered.

https://www.onlinelibrary.wiley.com/doi/epdf/10.1111/j.1469-8986.1997.tb02140.x

Heart rate variability: Origins, methods, and interpretive caveats

With continued debate over the functional significance of adult neurogenesis, identifying an in vivo correlate of neurogenesis has become an important goal. Here we rely on the coupling between neurogenesis and angiogenesis and test whether MRI measurements of cerebral blood volume (CBV) provide an imaging correlate of neurogenesis. First, we used an MRI approach to generate CBV maps over time in the hippocampal formation of exercising mice. Among all hippocampal subregions, exercise was found to have a primary effect on dentate gyrus CBV, the only subregion that supports adult neurogenesis. Moreover, exercise-induced increases in dentate gyrus CBV were found to correlate with postmortem measurements of neurogenesis. Second, using similar MRI technologies, we generated CBV maps over time in the hippocampal formation of exercising humans. As in mice, exercise was found to have a primary effect on dentate gyrus CBV, and the CBV changes were found to selectively correlate with cardiopulmonary and cognitive function. Taken together, these findings show that dentate gyrus CBV provides an imaging correlate of exercise-induced neurogenesis and that exercise differentially targets the dentate gyrus, a hippocampal subregion important for memory and implicated in cognitive aging.

/pdf/an-in-vivo-correlate-of-exercise-induced-neurogenesis-in-the-6gzlmr7ae0.pdf

An in vivo correlate of exercise-induced neurogenesis in the adult dentate gyrus.

https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(98)07376-0.pdf

Religion, spirituality, and medicine.

The entorhinal cortex has been implicated in the early stages of Alzheimer’s disease, which is characterized by changes in the tau protein and in the cleaved fragments of the amyloid precursor protein (APP) We used a high-resolution functional magnetic resonance imaging (fMRI) variant that can map metabolic defects in patients and mouse models to address basic questions about entorhinal cortex pathophysiology The entorhinal cortex is divided into functionally distinct regions, the medial entorhinal cortex (MEC) and the lateral entorhinal cortex (LEC), and we exploited the high-resolution capabilities of the fMRI variant to ask whether either of them was affected in patients with preclinical Alzheimer’s disease Next, we imaged three mouse models of disease to clarify how tau and APP relate to entorhinal cortex dysfunction and to determine whether the entorhinal cortex can act as a source of dysfunction observed in other cortical areas We found that the LEC was affected in preclinical disease, that LEC dysfunction could spread to the parietal cortex during preclinical disease and that APP expression potentiated tau toxicity in driving LEC dysfunction, thereby helping to explain regional vulnerability in the disease

/pdf/molecular-drivers-and-cortical-spread-of-lateral-entorhinal-2869e3xk1v.pdf

Molecular drivers and cortical spread of lateral entorhinal cortex dysfunction in preclinical Alzheimer's disease

https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(01)06803-9.pdf

Richard P. Sloan

Papers

An in vivo correlate of exercise-induced neurogenesis in the adult dentate gyrus.

Religion, spirituality, and medicine.

Molecular drivers and cortical spread of lateral entorhinal cortex dysfunction in preclinical Alzheimer's disease

Relation between depression after coronary artery bypass surgery and 12-month outcome: a prospective study.

Heart rate variability in depressive and anxiety disorders.