A 3-Month Aerobic Training Program Improves Brain Energy Metabolism in Mild Alzheimer’s Disease: Preliminary Results from a Neuroimaging Study

Castellano, Christian‐Alexandre; Paquet, Nancy; Dionne, Isabelle J.; Imbeault, Hélène; Langlois, Francis; Croteau, Étienne; Tremblay, Sébastien; Fortier, Mélanie; Matte, J. J.; Lacombe, Guy; Fülöp, Tamás; Bocti, Christian; Cunnane, Stephen C.

doi:10.3233/jad-161163

Cited by 50 publications

(30 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Ketones may counteract AD pathogenesis because a ketone ester diet that elevates BHB more than tenfold lessens Aβ and tau pathologies and ameliorates behavioural abnormalities in 3xTg-AD mice 143 . Moreover, Castellano et al recently reported that a 3-month aerobic training (brisk walking) programme increased brain cell ketone utilization in patients with AD threefold without affecting cerebral glucose utilization 144 , which may be one reason that aerobic exercise can protect the brain against AD. That IF may be another approach for subjects at risk of or with AD is suggested by a study using 11 C-acetoacetate positron emission tomography (PET) imaging that showed that within 48 hours of the onset of fasting, there is a sevenfold to eightfold increase in brain uptake of ketones 4,145 .…”

Section: Ims and Neurological Disordersmentioning

confidence: 99%

Intermittent metabolic switching, neuroplasticity and brain health

et al. 2018

View full text Add to dashboard Cite

During evolution, individuals whose brains and bodies functioned well in a fasted state were successful in acquiring food, enabling their survival and reproduction. With fasting and extended exercise, liver glycogen stores are depleted and ketones are produced from adipose-cell-derived fatty acids. This metabolic switch in cellular fuel source is accompanied by cellular and molecular adaptations of neural networks in the brain that enhance their functionality and bolster their resistance to stress, injury and disease. Here, we consider how intermittent metabolic switching, repeating cycles of a metabolic challenge that induces ketosis (fasting and/or exercise) followed by a recovery period (eating, resting and sleeping), may optimize brain function and resilience throughout the lifespan, with a focus on the neuronal circuits involved in cognition and mood. Such metabolic switching impacts multiple signalling pathways that promote neuroplasticity and resistance of the brain to injury and disease.

show abstract

Section: Ims and Neurological Disordersmentioning

confidence: 99%

Intermittent metabolic switching, neuroplasticity and brain health

et al. 2018

View full text Add to dashboard Cite

show abstract

“…Intermittent energy restriction improves cognitive and motor performance, and can protect neurons against dysfunction and degeneration in animal models of epilepsy, stroke, PD, and AD (Bruce-Keller et al, 1999; Duan and Mattson, 1999; Yu and Mattson, 1999; Halagappa et al, 2007; Alirezaei et al, 2010; Fann et al, 2014; Parikh et al, 2016; Prehn et al, 2017). Regular aerobic exercise, which is necessary for the survival of many animals, can also enhance brain health throughout the life course; exercise reduces anxiety and improves cognition in laboratory animals and human subjects (Intlekofer and Cotman, 2013; Boraxbekk et al, 2016; Castellano et al, 2017; Chirles et al, 2017; Raichlen and Alexander, 2017). While fasting and vigorous exercise are different challenges to the body and brain, emerging findings are revealing that they each elicit similar adaptive cellular responses that can enhance neuroplasticity and stress resistance.…”

Section: Metabolic Factors Can Accelerate or Decelerate Brain Agingmentioning

confidence: 99%

Hallmarks of Brain Aging: Adaptive and Pathological Modification by Metabolic States

2018

View full text Add to dashboard Cite

During aging, the cellular milieu of the brain exhibits tell-tale signs of compromised bioenergetics, impaired adaptive neuroplasticity and resilience, aberrant neuronal network activity, dysregulation of neuronal Ca2+ homeostasis, the accrual of oxidatively modified molecules and organelles, and inflammation. These alterations render the aging brain vulnerable to Alzheimer’s and Parkinson’s diseases and stroke. Emerging findings are revealing mechanisms by which sedentary overindulgent lifestyles accelerate brain aging, whereas lifestyles that include intermittent bioenergetic challenges (exercise, fasting, and intellectual challenges) foster healthy brain aging. Here we provide an overview of the cellular and molecular biology of brain aging, how those processes interface with disease-specific neurodegenerative pathways, and how metabolic states influence brain health.

show abstract

“…Therefore, regular physical exercise can be recommended as a prevention strategy for AD as well as one type of treatment for pre-clinical and late stage AD. Aerobic exercise in early AD is particularly associated with benefits in cognitive functioning [136,137,138]. …”

Section: The Effect Of Lifestyle and Diet On The Genesis/progressimentioning

confidence: 99%

The Role of Interleukin-18, Oxidative Stress and Metabolic Syndrome in Alzheimer’s Disease

Ojala

Sutinen

2017

JCM

View full text Add to dashboard Cite

The role of interleukins (ILs) and oxidative stress (OS) in precipitating neurodegenerative diseases including sporadic Alzheimer’s disease (AD), requires further clarification. In addition to neuropathological hallmarks—extracellular neuritic amyloid-β (Aβ) plaques, neurofibrillary tangles (NFT) containing hyperphosphorylated tau and neuronal loss—chronic inflammation, as well as oxidative and excitotoxic damage, are present in the AD brain. The pathological sequelae and the interaction of these events during the course of AD need further investigation. The brain is particularly sensitive to OS, due to the richness of its peroxidation-sensitive fatty acids, coupled with its high oxygen demand. At the same time, the brain lack robust antioxidant systems. Among the multiple mechanisms and triggers by which OS can accumulate, inflammatory cytokines can sustain oxidative and nitrosative stress, leading eventually to cellular damage. Understanding the consequences of inflammation and OS may clarify the initial events underlying AD, including in interaction with genetic factors. Inflammatory cytokines are potential inducers of aberrant gene expression through transcription factors. Susceptibility disorders for AD, including obesity, type-2 diabetes, cardiovascular diseases and metabolic syndrome have been linked to increases in the proinflammatory cytokine, IL-18, which also regulates multiple AD related proteins. The association of IL-18 with AD and AD-linked medical conditions are reviewed in the article. Such data indicates that an active lifestyle, coupled to a healthy diet can ameliorate inflammation and reduce the risk of sporadic AD.

show abstract

A 3-Month Aerobic Training Program Improves Brain Energy Metabolism in Mild Alzheimer’s Disease: Preliminary Results from a Neuroimaging Study

Abstract: In mild AD, aerobic training improved brain energy metabolism by increasing ketone uptake and utilization while maintaining brain glucose uptake, and could potentially be associated with some cognitive improvement.

Cited by 50 publications

References 54 publications

Intermittent metabolic switching, neuroplasticity and brain health

Intermittent metabolic switching, neuroplasticity and brain health

Hallmarks of Brain Aging: Adaptive and Pathological Modification by Metabolic States

The Role of Interleukin-18, Oxidative Stress and Metabolic Syndrome in Alzheimer’s Disease

Contact Info

Product

Resources

About