Physical and Mental Work Outs Help Manage Neurodegeneration

It seems there’s real benefit to be gained from keeping both body and mind active – even for neurodegenerative disease sufferers.

Here’s a list of references confirming scientific findings.

Neuroplasticity References – Value of Exercise in Neurological Diseases

http://www.ncbi.nlm.nih.gov/pubmed
Eur J Phys Rehabil Med. 2009 Jun;45(2):215-29.
Exercise and neuroplasticity in persons living with Parkinson’s disease.
Hirsch MA, Farley BG.Carolinas Rehabilitation, Department of Physical Medicine and Rehabilitation, Charlotte, North Carolina 28203, USA. mark.hirsch@carolinashealthcare.org

Abstract
For many years, exercise was not a recommended rehabilitation strategy for persons with a diagnosis of idiopathic Parkinson’s disease (PD). Since it was believed that exercise had no measurable effect on PD, or might worsen the underlying pathology, it was to be avoided. A rich vein of bench and translational research now suggest non-pharmacological approaches, such as exercise or physiotherapy, have a far greater effect on the cardinal features of PD than previously believed. In particular, recent studies utilizing animal models of PD have begun to explore the molecular mechanisms of exercise-induced changes in the pathophysiology of PD. Yet, many clinicians and communities remain unaware of the scientific literature underlying exercise-induced brain repair or reorganization (neuroplasticity) and accompanying behavioral recovery in animal models of PD. The authors will summarize some noteworthy preliminary studies suggesting that continuous, deficit targeted, intensive training may confer neuroprotection and thereby, slow, stop or reverse the progression of the disease or promote neurorestoration through adaptation of compromised signaling pathways. While much work remains and these preliminary results await replication in larger prospective human trials, we believe a major challenge in the field of non-pharmacological, rehabilitative intervention for PD will be the extent to which healthcare providers are able to translate the science of exercise and PD to the level of the community.

PMID: 19532109 [PubMed – indexed for MEDLINE]Free Article

http://www.ncbi.nlm.nih.gov/pubmed/18474414
Alzheimer’s disease, cerebrovascular dysfunction and the benefits of exercise: from vessels to neurons.
Lange-Asschenfeldt C, Kojda G.
Klinik für Psychiatrie und Psychotherapie, Abteilung Gerontopsychiatrie, Bergische Landstr. 2, Düsseldorf 40629, Germany.

Abstract

Exercise training promotes extensive cardiovascular changes and adaptive mechanisms in both the peripheral and cerebral vasculature, such as improved organ blood flow, induction of antioxidant pathways, and enhanced angiogenesis and vascular regeneration. Clinical studies have demonstrated a reduction of morbidity and mortality from cardiovascular disease among exercising individuals. However, evidence from recent large clinical trials also suggests a substantial reduction of dementia risk – particularly regarding Alzheimer’s disease (AD) – with regular exercise. Enhanced neurogenesis and improved synaptic plasticity have been implicated in this beneficial effect. However, recent research has revealed that vascular and specifically endothelial dysfunction is essentially involved in the disease process and profoundly aggravates underlying neurodegeneration. Moreover, vascular risk factors (VRFs) are probably determinants of incidence and course of AD. In this review, we emphasize the interconnection between AD and VRFs and the impact of cerebrovascular and endothelial dysfunction on AD pathophysiology. Furthermore, we describe the molecular mechanisms of the beneficial effects of exercise on the vasculature such as activation of the vascular nitric oxide (NO)/endothelial NO synthase (eNOS) pathway, upregulation of antioxidant enzymes, and angiogenesis. Finally, recent prospective clinical studies dealing with the effect of exercise on the risk of incident AD are briefly reviewed. We conclude that, next to upholding neuronal plasticity, regular exercise may counteract AD pathophysiology by building a vascular reserve.

PMID: 18474414 [PubMed – indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/19819293
The neurobiology of brain and cognitive reserve: mental and physical activity as modulators of brain disorders.
Nithianantharajah J, Hannan AJ.
Howard Florey Institute, Florey Neuroscience Institutes, University of Melbourne, Victoria 3010, Australia.
Abstract

The concept of ‘cognitive reserve’, and a broader theory of ‘brain reserve’, were originally proposed to help explain epidemiological data indicating that individuals who engaged in higher levels of mental and physical activity via education, occupation and recreation, were at lower risk of developing Alzheimer’s disease and other forms of dementia. Subsequently, behavioral, cellular and molecular studies in animals (predominantly mice and rats) have revealed dramatic effects of environmental enrichment, which involves enhanced levels of sensory, cognitive and motor stimulation via housing in novel, complex environments. Furthermore, increasing levels of voluntary physical exercise, via ad libitum access to running wheels, can have significant effects on brain and behavior, thus informing the relative effects of mental and physical activity. More recently, animal models of brain disorders have been compared under environmentally stimulating and standard housing conditions, and this has provided new insights into environmental modulators and gene-environment interactions involved in pathogenesis. Here, we review animal studies that have investigated the effects of modifying mental and physical activity via experimental manipulations, and discuss their relevance to brain and cognitive reserve (BCR). Recent evidence suggests that the concept of BCR is not only relevant to brain aging, neurodegenerative diseases and dementia, but also to other neurological and psychiatric disorders. Understanding the cellular and molecular mechanisms mediating BCR may not only facilitate future strategies aimed at optimising healthy brain aging, but could also identify molecular targets for novel pharmacological approaches aimed at boosting BCR in ‘at risk’ and symptomatic individuals with various brain disorders.

http://www.ncbi.nlm.nih.gov/pubmed/18045158
Neurogenesis in the adult brain: implications for Alzheimer’s disease.
Galvan V, Bredesen DE.
Buck Institute for Age Research, 8001 Redwood Blvd., Novato, CA 94945, USA.
Abstract

The function of neurogenesis in the adult brain is still unknown. Interventions such as environmental enrichment and exercise impinge on neurogenesis, suggesting that the process is regulated by experience. Conversely, a role for neurogenesis in learning has been proposed through ‘cellular plasticity’, a process akin to synaptic plasticity but operating at the network level. Although neurogenesis is stimulated by acute injury, and possibly by neurodegenerative processes such as Alzheimer’s disease (AD), it does not suffice to restore function. While the role and direction of change in the neurogenic response at different stages of AD is still a matter of debate, it is possible that a deficit in neurogenesis may contribute to AD pathogenesis since at least one of the two regions ostensibly neurogenic in the adult human brain (the subgranular zone of the dentage gyrus and the ventriculo-olfactory neurogenic system) support high-level functions affected in early AD (associative memory and olfaction respectively). The age of onset and the rate of progression of sporadic forms of AD are highly variable. Sporadic AD may have a component of insufficient neurogenic replacement or insufficient neurogenic stimulation that is correlated with traits of personal history; the rate of neurogenesis and the survival of replicating progenitors is strongly modified by behavioral interventions known to impinge on the rate of neurogenesis and the probability of survival of newly born neurons–exercise, enriched experience, and learning. This view is consistent with epidemiological data suggesting that higher education and increased participation in intellectual, social and physical aspects of daily life are associated with slower cognitive decline in healthy elderly (“cognitive reserve”) and may reduce the risk of AD. Although neurogenesis can be modulated exogenously by growth factors, stimulation of neurogenesis as a mean to treat neurodegeneration is still for the most part speculative. Moreover, it is possible that different roles of neurogenesis during the course of AD are dictated by the degree of permissibility of the environment in which the process is taking place. A unique opportunity may exist in which the therapeutic stimulation of neurogenesis might contribute to functional ‘repair’ of the adult diseased brain, before damage to whole neuronal networks has ensued. In spite of the considerable gaps in our knowledge of neurogenesis, and of the considerable limitations that will need to be overcome before we can intervene in the process, that new neurons are added continuously to the adult mammalian brain is a discovery that has already changed the way we think about neurobiology, and may soon change the way we understand and approach neurodegenerative diseases such as AD.

http://www.ncbi.nlm.nih.gov/pubmed/17629545
Capitalizing on cortical plasticity: influence of physical activity on cognition and brain function.
Kramer AF, Erickson KI.
Beckman Institute and Department of Psychology, University of Illinois, Urbana, IL 61801, USA. a-kramer@uiuc.edu
Abstract

Given the aging populations in many countries throughout the world, there is an increasing interest in lifestyle factors and interventions that will enhance the cognitive vitality of older adults and reduce the risk for age-related neurological disorders, such as Alzheimer’s disease. In this review, we evaluate the hypothesis that physical activity and exercise might serve to protect, and also enhance, cognitive and brain function across the adult lifespan. To this end, we critically review three separate literatures that have examined the influence of physical activity and exercise on cognition, brain function and brain structure of adults, including epidemiological or prospective observational studies, randomized human clinical interventions and non-human animal studies. We suggest that this literature supports the claim that physical activity enhances cognitive and brain function, and protects against the development of neurodegenerative diseases. We discuss future directions to address currently unresolved questions, such as interactions between multiple lifestyle factors on offsetting or protecting against cognitive and neural decline, and conclude that physical activity is an inexpensive treatment that could have substantial preventative and restorative properties for cognitive and brain function.

http://www.ncbi.nlm.nih.gov/pubmed/16648603
Neurobiology of exercise.
Dishman RK, Berthoud HR, Booth FW, Cotman CW, Edgerton VR, Fleshner MR, Gandevia SC, Gomez-Pinilla F, Greenwood BN,Hillman CH, Kramer AF, Levin BE, Moran TH, Russo-Neustadt AA, Salamone JD, Van Hoomissen JD, Wade CE, York DA, Zigmond MJ.
Department of Exercise Science, The University of Georgia, Ramsey Center, 330 River Road, Athens, GA 30602-6554, USA. rdishman@uga.edu
Abstract

Voluntary physical activity and exercise training can favorably influence brain plasticity by facilitating neurogenerative, neuroadaptive, and neuroprotective processes. At least some of the processes are mediated by neurotrophic factors. Motor skill training and regular exercise enhance executive functions of cognition and some types of learning, including motor learning in the spinal cord. These adaptations in the central nervous system have implications for the prevention and treatment of obesity, cancer, depression, the decline in cognition associated with aging, and neurological disorders such as Parkinson’s disease, Alzheimer’s dementia, ischemic stroke, and head and spinal cord injury. Chronic voluntary physical activity also attenuates neural responses to stress in brain circuits responsible for regulating peripheral sympathetic activity, suggesting constraint on sympathetic responses to stress that could plausibly contribute to reductions in clinical disorders such as hypertension, heart failure, oxidative stress, and suppression of immunity. Mechanisms explaining these adaptations are not as yet known, but metabolic and neurochemical pathways among skeletal muscle, the spinal cord, and the brain offer plausible, testable mechanisms that might help explain effects of physical activity and exercise on the central nervous system.

http://www.ncbi.nlm.nih.gov/pubmed/12815500
Cognitive reserve and lifestyle.
Scarmeas N, Stern Y.
Cognitive Neuroscience Division, Department of Neurology, Taub Institute for Research in Alzheimer’s Disease and the Aging Brain, and College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA. ns257@columbia.edu
Abstract

The concept of cognitive reserve (CR) suggests that innate intelligence or aspects of life experience like educational or occupational attainments may supply reserve, in the form of a set of skills or repertoires that allows some people to cope with progressing Alzheimer’s disease (AD) pathology better than others. There is epidemiological evidence that lifestyle characterized by engagement in leisure activities of intellectual and social nature is associated with slower cognitive decline in healthy elderly and may reduce the risk of incident dementia. There is also evidence from functional imaging studies that subjects engaging in such leisure activities can clinically tolerate more AD pathology. It is possible that aspects of life experience like engagement in leisure activities may result in functionally more efficient cognitive networks and therefore provide a CR that delays the onset of clinical manifestations of dementia.

PMID: 12815500 [PubMed – indexed for MEDLINE]PMCID: PMC3024591Free PMC Article

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