scholarly journals Long-term cyclic aerobic training preserves the brain's health in elderly persons (brief review)

2016 ◽  
Vol 24 (4) ◽  
pp. 152-163
Author(s):  
A S Radchenko ◽  
B B Davydov ◽  
A N Kalinichenko
Keyword(s):  
Aerobic Training ◽  
Brain Perfusion ◽  
Favorable Effect ◽  
Elderly Persons ◽  
Periodical Literature ◽  
Brain Health ◽  
Memory State ◽  
Age Related ◽  
The Brain

It was identified on the base of special periodical literature analyze that cyclic muscular work systematically performed during large part of the person's life (former athlete) provides mainly the favorable effect on the brain. Ventricular-arterial coupling improvement ameliorates brain perfusion, and creates function advantages to brain health in old age. At that, the gray and white matter fading hampered, especially in structures that associated with visual control and human body spatial orientation, motor control and memory state, and age-related attenuation of cognitive functions in comparison with sedentary persons of the same age.

Beyond Standard Anti-Dementia Therapies: Diet, Exercise, Socialization, and Supplements

CNS Spectrums ◽  
2008 ◽  
Vol 13 (S16) ◽  
pp. 31-33 ◽  
Author(s):  
Gary W. Small
Keyword(s):  
Glycemic Index ◽  
Lower Risk ◽  
Fruits And Vegetables ◽  
Genetic Factors ◽  
Caloric Intake ◽  
Epidemiologic Studies ◽  
Omega 3 ◽  
Brain Health ◽  
Age Related ◽  
The Brain

Several lines of evidence point to lifestyle choices that may improve brain health. Genetic factors are important to the process of aging, especially as it relates to vulnerability to Alzheimer’s disease (AD), but non-genetic factors clearly have a role as well. This paper highlights studies suggesting that diet, exercise, socialization, and supplements may protect the brain from age-related decline.Observational evidence has indicated that several dietary practices can help maintain the health of one’s brain. The first such practice is to moderate one’s caloric intake. Illnesses related to obesity, such as diabetes, hypertension, and high cholesterol, are associated with poorer brain health. The second is to increase one’s intake of antioxidant foods, such as fresh fruits, and vegetables. The third is to increase intake of foods rich in omega-3 fatty acids, such as fish and olive oil. These fats in the diet may be associated with lower risk of dementia. Finally, consuming low glycemic-index carbohydrates instead of high glycemic-index carbohydrates, which spike blood sugar levels and are associated with higher risk of type 2 diabetes, may benefit the brain.Many studies have been conducted on the connection between a lower risk for AD and healthy diet. While there are not much data from randomized-controlled trials, epidemiologic studies support the theory that diet can have an impact on vulnerability to AD.

scholarly journals Mitigating Long-Term COVID-19 Consequences on Brain Health

2021 ◽  
Vol 12 ◽  
Author(s):  
Ryan C. N. D'Arcy ◽  
Jagdeep K. Sandhu ◽  
Shawn Marshall ◽  
Markus Besemann
Keyword(s):  
Risk Factors ◽  
Nervous System ◽  
Digital Health ◽  
Objective Evaluation ◽  
Health Impacts ◽  
Brain Health ◽  
Health Innovations ◽  
Starting Point ◽  
The Brain

COVID-19 is increasingly being linked to brain health impacts. The emerging situation is consistent with evidence of immunological injury to the brain, which has been described as a resulting “brain fog.” The situation need not be medicalized but rather clinically managed in terms of improving resilience for an over-stressed nervous system. Pre-existing comparisons include managing post-concussion syndromes and/or brain fog. The objective evaluation of changes in cognitive functioning will be an important clinical starting point, which is being accelerated through pandemic digital health innovations. Pre-morbid brain health can significantly optimize risk factors and existing clinical frameworks provide useful guidance in managing over-stressed COVID-19 nervous systems.

scholarly journals Reward enhances memory via age-varying online and offline neural mechanisms across development

2021 ◽  
Author(s):  
Alexandra O Cohen ◽  
Morgan M Glover ◽  
Xinxu Shen ◽  
Camille V Phaneuf ◽  
Kristen N Avallone ◽  
...  
Keyword(s):  
Associative Memory ◽  
Neural Circuits ◽  
Neural Mechanisms ◽  
Age Related ◽  
High Reward ◽  
Memory Representations ◽  
Dopamine Signaling ◽  
Reward Motivation ◽  
The Brain

Reward motivation enhances memory through interactions between mesolimbic, hippocampal, and cortical systems - both during and after encoding. Developmental changes in these distributed neural circuits may lead to age-related differences in reward-motivated memory and the underlying neural mechanisms. Converging evidence from cross-species studies suggests that subcortical dopamine signaling is increased during adolescence, which may lead to stronger memory representations of rewarding, relative to mundane, events and changes in the contributions of underlying subcortical and cortical brain mechanisms across age. Here, we used fMRI to examine how reward motivation influences the "online" encoding and "offline" post-encoding brain mechanisms that support long-term associative memory from childhood to adulthood. We found that reward motivation led to both age-invariant as well as adolescent-specific enhancements in associative memory after 24 hours. Furthermore, reward-related memory benefits were linked to age-varying neural mechanisms. During encoding, interactions between the prefrontal cortex and ventral tegmental area (VTA) were associated with better high-reward memory to a greater degree with increasing age. Pre- to post-encoding changes in functional connectivity between the anterior hippocampus and VTA were also associated with better high-reward memory, but more so at younger ages. Our findings suggest that there may be developmental shifts - from offline subcortical to online cortical processes - in the brain mechanisms supporting reward-motivated memory.

scholarly journals Multiple Causes of Dementia as Engineered Senescence

2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Mario Dominic Garrett
Keyword(s):  
Antagonistic Pleiotropy ◽  
Misfolded Protein ◽  
Optimal Conditions ◽  
Short Term ◽  
Trade Off ◽  
Age Related ◽  
The Many ◽  
Biology Of Aging ◽  
The Brain

All traumas—cranial, cardiovascular, hormone, viral, bacterial, fungi, parasites, misfolded protein, genetic, behavior, environmental and medication—affect the brain. This paper itemizes studies showing the many different causes of dementia including Alzheimer’s disease. Causes interact with each other, act sequentially by preparing the optimal conditions for its successor, initiate other diseases, allow for other traumas to accumulate and degrade protective features of the brain. Since such age-related cognitive impairment is not exclusively a human attribute there might be support for an evolutionary theory of dementia. Relying on theories of antagonistic pleiotropy and polymorphism, the brain has been designed to sequester trauma. Because of increased longevity, the short-term tactic of sequestering trauma becomes a long-term liability. We are engineered to sequester these insults until a tipping point is reached. Dementia is an evolutionary trade-off for longevity. We cannot cure dementia without understanding the overall biology of aging.

scholarly journals Understanding the Potential Role of Sirtuin 2 on Aging: Consequences of SIRT2.3 Overexpression in Senescence

2021 ◽  
Vol 22 (6) ◽  
pp. 3107
Author(s):  
Noemi Sola-Sevilla ◽  
Ana Ricobaraza ◽  
Ruben Hernandez-Alcoceba ◽  
Maria S. Aymerich ◽  
Rosa M. Tordera ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Potential Role ◽  
Adeno Associated Virus ◽  
Age Related ◽  
Age Dependent ◽  
Molecular Effects ◽  
Samp8 Mice ◽  
The Brain

Sirtuin 2 (SIRT2) has been associated to aging and age-related pathologies. Specifically, an age-dependent accumulation of isoform 3 of SIRT2 in the CNS has been demonstrated; however, no study has addressed the behavioral or molecular consequences that this could have on aging. In the present study, we have designed an adeno-associated virus vector (AAV-CAG-Sirt2.3-eGFP) for the overexpression of SIRT2.3 in the hippocampus of 2 month-old SAMR1 and SAMP8 mice. Our results show that the specific overexpression of this isoform does not induce significant behavioral or molecular effects at short or long term in the control strain. Only a tendency towards a worsening in the performance in acquisition phase of the Morris Water Maze was found in SAMP8 mice, together with a significant increase in the pro-inflammatory cytokine Il-1β. These results suggest that the age-related increase of SIRT2.3 found in the brain is not responsible for induction or prevention of senescence. Nevertheless, in combination with other risk factors, it could contribute to the progression of age-related processes. Understanding the specific role of SIRT2 on aging and the underlying molecular mechanisms is essential to design new and more successful therapies for the treatment of age-related diseases.

scholarly journals Mapping the collaterome for precision cerebrovascular health: Theranostics in the continuum of stroke and dementia

2017 ◽  
Vol 38 (9) ◽  
pp. 1449-1460 ◽  
Author(s):  
David S Liebeskind
Keyword(s):  
Large Scale ◽  
Clinical Implications ◽  
Brain Health ◽  
Ischemic Brain ◽  
Arterial Inflow ◽  
Cerebrovascular Health ◽  
The Brain ◽  
Long Term Preservation

Precision cerebrovascular health or individualized long-term preservation of the brain and associated blood vessels, is predicated on understanding, diagnosing, and tailoring therapies for people at risk of ischemic injury associated with stroke and vascular dementia. The associated imaging patterns are sculpted by the protective effect of the collaterome, the innate compensatory ability of the brain and vasculature to offset hypoperfusion when antegrade or normal arterial inflow pathways are compromised. Theranostics or rational and synchronous use of diagnostic studies in tandem with specific therapies to optimally guide patient outcomes in ischemic brain disorders may capitalize on the pivotal role of the collaterome. Understanding the functional impact of the collaterome across populations of individuals would advance translational science on the brain, while questions with immediate clinical implications may be prioritized. Big data and systematic analyses are necessary to develop normative standards, multimodal imaging atlases, and delineation of specific patterns to guide clinical management. Large-scale, systematic imaging analyses of the collaterome provide a platform for translational work on cerebral collateral circulation and hemodynamics and a theranostic framework with direct clinical implications. This article frames incipient research objectives to guide precision stroke medicine in coming years, building upon the collaterome concept in brain health.

scholarly journals Potential Moderators of Physical Activity on Brain Health

2012 ◽  
Vol 2012 ◽  
pp. 1-14 ◽  
Author(s):  
Regina L. Leckie ◽  
Andrea M. Weinstein ◽  
Jennifer C. Hodzic ◽  
Kirk I. Erickson
Keyword(s):  
Physical Activity ◽  
Brain Dysfunction ◽  
Future Research ◽  
Omega 3 ◽  
Brain Health ◽  
Functional Changes ◽  
Age Related ◽  
Genetic Risks ◽  
The Individual ◽  
The Brain

Age-related cognitive decline is linked to numerous molecular, structural, and functional changes in the brain. However, physical activity is a promising method of reducing unfavorable age-related changes. Physical activity exerts its effects on the brain through many molecular pathways, some of which are regulated by genetic variants in humans. In this paper, we highlight genes including apolipoprotein E (APOE), brain derived neurotrophic factor (BDNF), and catechol-O-methyltransferase (COMT) along with dietary omega-3 fatty acid, docosahexaenoic acid (DHA), as potential moderators of the effect of physical activity on brain health. There are a growing number of studies indicating that physical activity might mitigate the genetic risks for disease and brain dysfunction and that the combination of greater amounts of DHA intake with physical activity might promote better brain function than either treatment alone. Understanding whether genes or other lifestyles moderate the effects of physical activity on neurocognitive health is necessary for delineating the pathways by which brain health can be enhanced and for grasping the individual variation in the effectiveness of physical activity interventions on the brain and cognition. There is a need for future research to continue to assess the factors that moderate the effects of physical activity on neurocognitive function.

scholarly journals Hippocampal Growth Factor and Myokine Cathepsin B Expression following Aerobic and Resistance Training in 3xTg-AD Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-11 ◽  
Author(s):  
Gabriel S. Pena ◽  
Hector G. Paez ◽  
Trevor K. Johnson ◽  
Jessica L. Halle ◽  
Joseph P. Carzoli ◽  
...  
Keyword(s):  
Resistance Training ◽  
Brain Function ◽  
Cathepsin B ◽  
Aerobic Training ◽  
Treadmill Running ◽  
Direct Effects ◽  
Brain Health ◽  
Training Modalities ◽  
The Brain

Aerobic training (AT) can support brain health in Alzheimer’s disease (AD); however, the role of resistance training (RT) in AD is not well established. Aside from direct effects on the brain, exercise may also regulate brain function through secretion of muscle-derived myokines. Aims. This study examined the effects of AT and RT on hippocampal BDNF and IGF-1 signaling, β-amyloid expression, and myokine cathepsin B in the triple transgenic (3xTg-AD) model of AD. 3xTg-AD mice were assigned to one of the following groups: sedentary (Tg), aerobic trained (Tg+AT, 9 wks treadmill running), or resistance trained (Tg+RT, 9 wks weighted ladder climbing) (n=10/group). Rotarod latency and strength were assessed pre- and posttraining. Hippocampus and skeletal muscle were collected after training and analyzed by high-resolution respirometry, ELISA, and immunoblotting. Tg+RT showed greater grip strength than Tg and Tg+AT at posttraining (p<0.01). Only Tg+AT improved rotarod peak latency (p<0.01). Hippocampal IGF-1 concentration was ~15% greater in Tg+AT and Tg+RT compared to Tg (p<0.05); however, downstream signals of p-IGF-1R, p-Akt, p-MAPK, and p-GSK3β were not altered. Cathepsin B, hippocampal p-CREB and BDNF, and hippocampal mitochondrial respiration were not affected by AT or RT. β-Amyloid was ~30% lower in Tg+RT compared to Tg (p<0.05). This data suggests that regular resistance training reduces β-amyloid in the hippocampus concurrent with increased concentrations of IGF-1. Both types of training offered distinct benefits, either by improving physical function or by modifying signals in the hippocampus. Therefore, inclusion of both training modalities may address central defects, as well as peripheral comorbidities in AD.

scholarly journals Postweaning Iron Deficiency in Male Rats Leads to Long-Term Hyperactivity and Decreased Reelin Gene Expression in the Nucleus Accumbens

2019 ◽  
Author(s):  
Noriko Nishikura ◽  
Kodai Hino ◽  
Tomoko Kimura ◽  
Yasuhiro Uchimura ◽  
Shinjiro Hino ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nucleus Accumbens ◽  
Iron Deficiency ◽  
Male Rats ◽  
Juvenile Period ◽  
Synaptic Density ◽  
Adequate Diet ◽  
Age Related ◽  
The Brain

ABSTRACT Background Epidemiological research indicates that iron deficiency (ID) in infancy correlates with long-term cognitive impairment and behavioral disturbances, despite therapy. However, the mechanisms underlying these effects are unknown. Objective We investigated how ID affected postweaning behavior and monoamine concentration in rat brains to determine whether ID during the juvenile period affected gene expression and synapse formation in the prefrontal cortex (PFC) and nucleus accumbens (NAcc). Methods Fischer 344/Jcl postweaning male rats aged 21–39 d were fed low-iron diets (0.35 mg/kg iron; ID group) or standard AIN-93 G diets [3.5 mg/kg iron; control (CN) group]. After day 39, all rats were fed the iron-adequate diet. The locomotor activity was evaluated by the open field and elevated plus maze tests at 8 and 12 wk of age. Monoamine concentrations in the brain were analyzed using HPLC at 9 and 13 wk of age. Comprehensive gene expression analysis was performed in the PFC and NAcc at 13 wk of age. Finally, we investigated synaptic density in the PFC and NAcc by synaptophysin immunostaining. Results Behavioral tests revealed a significant reduction of the age-related decline in the total distance traveled in ID rats compared with CN rats (P < 0.05), indicating that ID affected hyperactivity, which persisted into adulthood (13 wk of age). At this age, reelin (Reln) mRNA expression (adjusted P < 0.01) decreased and synaptic density (P < 0.01) increased in the NAcc in the ID group. Regarding the mesolimbic pathway, homovanillic acid concentration increased in the NAcc, whereas the dopamine concentration decreased in the ventral midbrain. Conclusions Our results suggest that ID during the postweaning period in male rats, despite complete iron repletion following ID, led to long-term hyperactivity via monoamine disturbance in the brain and an alteration in the synaptic plasticity accompanied by downregulation of Reln expression in the NAcc.

“Brainstorming”: Extracellular Vesicles in Physical Activity and Neuronal Health

2020 ◽  
Vol 2 (1) ◽  
pp. 54-59
Author(s):  
Alexandra Brahmer ◽  
Eva-Maria Krämer-Albers
Keyword(s):  
Physical Activity ◽  
Extracellular Vesicles ◽  
Well Being ◽  
Brain Health ◽  
Communication Processes ◽  
And Function ◽  
Complex Architecture ◽  
Neuronal Maintenance ◽  
The Brain

Physical and mental activity are known to contribute to brain health and overall longevity. Extracellular vesicles (EVs) have attracted attention for their ability to transport bioactive cargo through various body-fluids and their role in tissue crosstalk and regeneration. Targeted intercellular communication processes, including those facilitated by EVs, are of vital importance for the complex architecture and function of the brain. Activated neurons trigger the transfer of EVs from myelinating oligodendrocytes to neurons, promoting neuronal long-term maintenance and survival. Likewise, physical activity leads to the liberation of EVs into the circulation, while the molecular link between physical activity and neural performance is not yet fully understood. Interestingly, there are indications that EVs might be able to overcome the blood-brain-barrier and affect neuronal cells. Here, we discuss the ability of EVs to “storm the brain” in response to neural and physical activity in benefit of well-being and sustained brain health. Keywords: oligodendrocytes, neuron-glia interaction, extracellular vesicles, physical exercise, neuronal maintenance, neuroprotection

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