Proceedings from the Albert Charitable Trust Inaugural Workshop on ‘Understanding the Acute Effects of Exercise on the Brain’

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Abstract

An inaugural workshop supported by “The Leo and Anne Albert Charitable Trust,” was held October 4–7, 2019 in Scottsdale, Arizona, to focus on the effects of exercise on the brain and to discuss how physical activity may prevent or delay the onset of aging-related neurodegenerative conditions. The Scientific Program Committee (led by Dr. Jeff Burns) assembled translational, clinical, and basic scientists who research various aspects of the effects of exercise on the body and brain, with the overall goal of gaining a better understanding as to how to delay or prevent neurodegenerative diseases. In particular, research topics included the links between cardiorespiratory fitness, the cerebrovasculature, energy metabolism, peripheral organs, and cognitive function, which are all highly relevant to understanding the effects of acute and chronic exercise on the brain. The Albert Trust workshop participants addressed these and related topics, as well as how other lifestyle interventions, such as diet, affect age-related cognitive decline associated with Alzheimer’s and other neurodegenerative diseases. This report provides a synopsis of the presentations and discussions by the participants, and a delineation of the next steps towards advancing our understanding of the effects of exercise on the aging brain.

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Most cited references 142

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Exercise training increases size of hippocampus and improves memory.

K. I. Erickson, M. Voss, R Prakash … (2011)

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.

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Gut microbiome alterations in Alzheimer’s disease

Nicholas Vogt, Robert Kerby, Kimberly Dill-McFarland … (2017)

Alzheimer’s disease (AD) is the most common form of dementia. However, the etiopathogenesis of this devastating disease is not fully understood. Recent studies in rodents suggest that alterations in the gut microbiome may contribute to amyloid deposition, yet the microbial communities associated with AD have not been characterized in humans. Towards this end, we characterized the bacterial taxonomic composition of fecal samples from participants with and without a diagnosis of dementia due to AD. Our analyses revealed that the gut microbiome of AD participants has decreased microbial diversity and is compositionally distinct from control age- and sex-matched individuals. We identified phylum- through genus-wide differences in bacterial abundance including decreased Firmicutes, increased Bacteroidetes, and decreased Bifidobacterium in the microbiome of AD participants. Furthermore, we observed correlations between levels of differentially abundant genera and cerebrospinal fluid (CSF) biomarkers of AD. These findings add AD to the growing list of diseases associated with gut microbial alterations, as well as suggest that gut bacterial communities may be a target for therapeutic intervention.

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Potential for primary prevention of Alzheimer's disease: an analysis of population-based data.

Sam Norton, Fiona Matthews, Deborah Barnes … (2014)

Recent estimates suggesting that over half of Alzheimer's disease burden worldwide might be attributed to potentially modifiable risk factors do not take into account risk-factor non-independence. We aimed to provide specific estimates of preventive potential by accounting for the association between risk factors. Using relative risks from existing meta-analyses, we estimated the population-attributable risk (PAR) of Alzheimer's disease worldwide and in the USA, Europe, and the UK for seven potentially modifiable risk factors that have consistent evidence of an association with the disease (diabetes, midlife hypertension, midlife obesity, physical inactivity, depression, smoking, and low educational attainment). The combined PAR associated with the risk factors was calculated using data from the Health Survey for England 2006 to estimate and adjust for the association between risk factors. The potential of risk factor reduction was assessed by examining the combined effect of relative reductions of 10% and 20% per decade for each of the seven risk factors on projections for Alzheimer's disease cases to 2050. Worldwide, the highest estimated PAR was for low educational attainment (19·1%, 95% CI 12·3-25·6). The highest estimated PAR was for physical inactivity in the USA (21·0%, 95% CI 5·8-36·6), Europe (20·3%, 5·6-35·6), and the UK (21·8%, 6·1-37·7). Assuming independence, the combined worldwide PAR for the seven risk factors was 49·4% (95% CI 25·7-68·4), which equates to 16·8 million attributable cases (95% CI 8·7-23·2 million) of 33·9 million cases. However, after adjustment for the association between the risk factors, the estimate reduced to 28·2% (95% CI 14·2-41·5), which equates to 9·6 million attributable cases (95% CI 4·8-14·1 million) of 33·9 million cases. Combined PAR estimates were about 30% for the USA, Europe, and the UK. Assuming a causal relation and intervention at the correct age for prevention, relative reductions of 10% per decade in the prevalence of each of the seven risk factors could reduce the prevalence of Alzheimer's disease in 2050 by 8·3% worldwide. After accounting for non-independence between risk factors, around a third of Alzheimer's diseases cases worldwide might be attributable to potentially modifiable risk factors. Alzheimer's disease incidence might be reduced through improved access to education and use of effective methods targeted at reducing the prevalence of vascular risk factors (eg, physical inactivity, smoking, midlife hypertension, midlife obesity, and diabetes) and depression. National Institute for Health Research Collaboration for Leadership in Applied Health Research and Care for Cambridgeshire and Peterborough. Copyright © 2014 Elsevier Ltd. All rights reserved.

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Author and article information

Journal

Journal ID (nlm-ta): Brain Plast

Journal ID (iso-abbrev): Brain Plast

Journal ID (publisher-id): BPL

Title: Brain Plasticity

Publisher: IOS Press (Nieuwe Hemweg 6B, 1013 BG Amsterdam, The Netherlands )

ISSN (Print): 2213-6304

ISSN (Electronic): 2213-6312

Publication date (Electronic, preprint): 05 December 2022

Publication date (Electronic, pub): 20 December 2022

Publication date (Electronic, collection): 2022

Volume: 8

Issue: 2

Pages: 153-168

Affiliations

[a ]Department of Kinesiology, University of Wisconsin-Madison , Madison, WI, USA

[b ]University of Kansas Alzheimer’s Disease Research Center , Fairway, KS, USA

[c ]UAB Center for Exercise Medicine, University of Alabama , Birmingham, AL, USA

[d ]Department of Internal Medicine, Division of Endocrinology and Metabolism, University of Iowa Carver College of Medicine , Iowa City, IA, USA

[e ]Department of Biomedical Sciences, University of Missouri , Columbia, MO, USA

[f ]Department of Kinesiology, Faculty of Medicine, Université Laval, and Research center of the Institut universitaire de cardiologie et de pneumologie de Québec , Québec city, QC, Canada

[g ]Department of Professional and Medical Education, Meharry Medical College , Nashville, TN, USA

[h ]Department of Kinesiology, University of Texas at Arlington , Arlington, Texas, USA

[i ]Department of Molecular and Integrative Physiology, University of Kansas Medical Center , Kansas City, KS, USA

[j ]University of Pittsburgh School of Medicine , Department of Psychiatry, Pittsburgh, PA, USA

[k ]School of Kinesiology, University of Michigan , Ann Arbor, MI, USA

[l ]Human and Evolutionary Biology Section, Department of Biological Sciences, Dornsrife College of Letters, Arts and Sciences, University of Southern California , Los Angeles, CA, USA

[m ]Aging and Metabolism Research Program, Oklahoma Medical Research Foundation , Oklahoma City, OK, USA

[n ]The Jackson Laboratory, Bar Harbor, ME, USA

[o ]Departments of Kinesiology, Anatomy and Physiology, Kansas State University , Manhattan, KS, USA

[p ]University of Colorado , Anschutz Medical Campus, Aurora, CO, USA

[q ]Department of Kinesiology, School of Public Health, University of Maryland , College Park, MD, USA

[r ]Vulnerable Brain Laboratory, Department Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University , London, N6A 5C1, Canada

[s ]Stiles-Nicholson Brain Institute, Charles E. Schmidt College of Medicine, Florida Atlantic University , Jupiter FL, USA

Author notes

[* ]Correspondence to: Henriette van Praag, Stiles-Nicholson Brain Institute, Charles E. Schmidt College of Medicine, Florida Atlantic University, Jupiter FL 33458, USA. E-mail: hvanpraag@ 123456health.fau.edu .

Article

Publisher ID: BPL220146

DOI: 10.3233/BPL-220146

PMC ID: 9837736

PubMed ID: 36721393

SO-VID: 92edef28-00aa-4dda-9bf1-d126633f929d

License:

This is an open access article distributed under the terms of the Creative Commons Attribution Non-Commercial (CC BY-NC 4.0) License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date accepted : 18 November 2022

Proceedings from the Albert Charitable Trust Inaugural Workshop on ‘Understanding the Acute Effects of Exercise on the Brain’

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Karger: Neurology and Neuroscience

Most cited references 142

Exercise training increases size of hippocampus and improves memory.

Gut microbiome alterations in Alzheimer’s disease

Potential for primary prevention of Alzheimer's disease: an analysis of population-based data.

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