scholarly journals The aging mind: neuroplasticity in response to cognitive training

2013 ◽  
Vol 15 (1) ◽  
pp. 109-119 ◽  
Keyword(s):  
Cognitive Function ◽  
Cognitive Training ◽  
Neural Plasticity ◽  
Cognitive Effort ◽  
Aging Brain ◽  
Cognitive Domains ◽  
Training Techniques ◽  
Age Related ◽  
Strategy Change ◽  
The Brain

Is it possible to enhance neural and cognitive function with cognitive training techniques? Can we delay age-related decline in cognitive function with interventions and stave off Alzheimer's disease? Does an aged brain really have the capacity to change in response to stimulation? In the present paper, we consider the neuroplasticity of the aging brain, that is, the brain's ability to increase capacity in response to sustained experience. We argue that, although there is some neural deterioration that occurs with age, the brain has the capacity to increase neural activity and develop neural scaffolding to regulate cognitive function. We suggest that increase in neural volume in response to cognitive training or experience is a clear indicator of change, but that changes in activation in response to cognitive training may be evidence of strategy change rather than indicative of neural plasticity. We note that the effect of cognitive training is surprisingly durable over time, but that the evidence that training effects transfer to other cognitive domains is relatively limited. We review evidence which suggests that engagement in an environment that requires sustained cognitive effort may facilitate cognitive function.

Age-related Shift in Neural Complexity Related to Task Performance and Physical Activity

2015 ◽  
Vol 27 (3) ◽  
pp. 605-613 ◽  
Author(s):  
Jennifer J. Heisz ◽  
Michelle Gould ◽  
Anthony R. McIntosh
Keyword(s):  
Physical Activity ◽  
Older Adults ◽  
Information Processing ◽  
Cognitive Function ◽  
Neural Plasticity ◽  
Structural Changes ◽  
Local Information ◽  
Multiscale Entropy ◽  
Age Related ◽  
The Brain

The human brain undergoes marked structural changes with age including cortical thinning and reduced connectivity because of the degradation of myelin. Although these changes can compromise cognitive function, the brain is able to functionally reorganize to compensate for some of this structural loss. However, there are interesting individual differences in outcome: When comparing individuals of similar age, those who engage in regular physical activity are less affected by the typical age-related decline in cognitive function. This study used multiscale entropy to reveal a shift in the way the brain processes information in older adults that is related to physical activity. Specifically, older adults who were more physically active engaged in more local neural information processing. Interestingly, this shift toward local information processing was also associated with improved executive function performance in older adults, suggesting that physical activity may help to improve aspects of cognitive function in older adults by biasing the neural system toward local information processing. In the face of age-related structural decline, the neural plasticity that is enhanced through physical activity may help older adults maintain cognitive health longer into their lifespan.

Exercise Impacts Age-Related Changes in Cognitive Function and Neural Complexity

2016 ◽  
Vol 5 (1) ◽  
pp. 30-38 ◽  
Author(s):  
Jennifer J. Heisz ◽  
Ana Kovacevic
Keyword(s):  
Older Adults ◽  
Cognitive Function ◽  
Executive Functions ◽  
Cognitive Outcomes ◽  
Physically Active ◽  
Age Related ◽  
The Neural Network ◽  
Future Work ◽  
The Brain ◽  
Age Related Changes

Age-related changes in the brain can compromise cognitive function. However, in some cases, the brain is able to functionally reorganize to compensate for some of this loss. The present paper reviews the benefits of exercise on executive functions in older adults and discusses a potential mechanism through which exercise may change the way the brain processes information for better cognitive outcomes. Specifically, older adults who are more physically active demonstrate a shift toward local neural processing that is associated with better executive functions. We discuss the use of neural complexity as a sensitive measure of the neural network plasticity that is enhanced through exercise. We conclude by highlighting the future work needed to improve exercise prescriptions that help older adults maintain their cognitive and physical functions for longer into their lifespan.

scholarly journals Disparate Central and Peripheral Effects of Circulating IGF-1 Deficiency on Tissue Mitochondrial Function

2019 ◽  
Vol 57 (3) ◽  
pp. 1317-1331 ◽  
Author(s):  
Gavin Pharaoh ◽  
Daniel Owen ◽  
Alexander Yeganeh ◽  
Pavithra Premkumar ◽  
Julie Farley ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Function ◽  
Spatial Learning ◽  
Mitochondrial Function ◽  
Coupling Efficiency ◽  
Redox Status ◽  
Cellular Aging ◽  
Age Related ◽  
The Brain ◽  
Circulating Levels

AbstractAge-related decline in circulating levels of insulin-like growth factor (IGF)-1 is associated with reduced cognitive function, neuronal aging, and neurodegeneration. Decreased mitochondrial function along with increased reactive oxygen species (ROS) and accumulation of damaged macromolecules are hallmarks of cellular aging. Based on numerous studies indicating pleiotropic effects of IGF-1 during aging, we compared the central and peripheral effects of circulating IGF-1 deficiency on tissue mitochondrial function using an inducible liver IGF-1 knockout (LID). Circulating levels of IGF-1 (~ 75%) were depleted in adult male Igf1f/f mice via AAV-mediated knockdown of hepatic IGF-1 at 5 months of age. Cognitive function was evaluated at 18 months using the radial arm water maze and glucose and insulin tolerance assessed. Mitochondrial function was analyzed in hippocampus, muscle, and visceral fat tissues using high-resolution respirometry O2K as well as redox status and oxidative stress in the cortex. Peripherally, IGF-1 deficiency did not significantly impact muscle mass or mitochondrial function. Aged LID mice were insulin resistant and exhibited ~ 60% less adipose tissue but increased fat mitochondrial respiration (20%). The effects on fat metabolism were attributed to increases in growth hormone. Centrally, IGF-1 deficiency impaired hippocampal-dependent spatial acquisition as well as reversal learning in male mice. Hippocampal mitochondrial OXPHOS coupling efficiency and cortex ATP levels (~ 50%) were decreased and hippocampal oxidative stress (protein carbonylation and F2-isoprostanes) was increased. These data suggest that IGF-1 is critical for regulating mitochondrial function, redox status, and spatial learning in the central nervous system but has limited impact on peripheral (liver and muscle) metabolism with age. Therefore, IGF-1 deficiency with age may increase sensitivity to damage in the brain and propensity for cognitive deficits. Targeting mitochondrial function in the brain may be an avenue for therapy of age-related impairment of cognitive function. Regulation of mitochondrial function and redox status by IGF-1 is essential to maintain brain function and coordinate hippocampal-dependent spatial learning. While a decline in IGF-1 in the periphery may be beneficial to avert cancer progression, diminished central IGF-1 signaling may mediate, in part, age-related cognitive dysfunction and cognitive pathologies potentially by decreasing mitochondrial function.

A Review and Reappraisal of the Default Network in Normal Aging and Dementia

2019 ◽  
Author(s):  
Jessica R. Andrews-Hanna ◽  
Matthew D. Grilli ◽  
Muireann Irish
Keyword(s):  
Older Adults ◽  
Cognitive Function ◽  
Brain Aging ◽  
Strong Support ◽  
Well Being ◽  
Normal Aging ◽  
Aging Brain ◽  
Default Network ◽  
Pathological Aging ◽  
Age Related

The brain’s default network (DN) has received considerable interest in the context of so-called “normal” and pathological aging. Findings have generally been couched in support of a pessimistic view of brain aging, marked by substantial loss of structural brain integrity accompanied by a host of impairments in brain and cognitive function. A critical look at the literature, however, reveals that the standard loss of integrity, loss of function (LILF) view in normal aging may not necessarily hold with respect to the DN and the internally guided functions it supports. Many internally guided processes subserved by the DN are preserved or enhanced in cognitively healthy older adults. Moreover, differences in motivational, contextual, and physiological factors between young and older adults likely influence the extant neuroimaging and cognitive findings. Accordingly, normal aging can be viewed as a series of possibly adaptive cognitive and DN-related alterations that bolster cognitive function and promote socioemotional well-being and stability in a stage of life noted for change. On the other hand, the available evidence reveals strong support for the LILF view of the DN in neurodegenerative disorders, whereby syndromes such as Alzheimer’s disease (AD) and semantic dementia (SD), characterized by progressive atrophy to distinct DN subsystems, display distinct aberrations in autobiographical and semantic cognition. Taken together, these findings call for more naturalistic, age-appropriate, and longitudinal paradigms when investigating neurocognitive changes in aging and to adequately assess and control for differences in non-neural factors that may obscure “true” effects of normal and pathological aging. A shift in the framework with which age-related alterations in internally guided cognition are interpreted may shed important light on the neurocognitive mechanisms differentiating healthy and pathological aging, leading to a more complete picture of the aging brain in all its complexity.

scholarly journals Impaired Mitophagy in Neurons and Glial Cells during Aging and Age-Related Disorders

2021 ◽  
Vol 22 (19) ◽  
pp. 10251
Author(s):  
Vladimir Sukhorukov ◽  
Dmitry Voronkov ◽  
Tatiana Baranich ◽  
Natalia Mudzhiri ◽  
Alina Magnaeva ◽  
...  
Keyword(s):  
Glial Cells ◽  
Brain Aging ◽  
Cellular Level ◽  
Aging Brain ◽  
The Past ◽  
Age Related ◽  
Accumulation Of Damage ◽  
Quantity Control ◽  
The Brain

Aging is associated with a decline in cognitive function, which can partly be explained by the accumulation of damage to the brain cells over time. Neurons and glia undergo morphological and ultrastructure changes during aging. Over the past several years, it has become evident that at the cellular level, various hallmarks of an aging brain are closely related to mitophagy. The importance of mitochondria quality and quantity control through mitophagy is highlighted by the contribution that defects in mitochondria–autophagy crosstalk make to aging and age-related diseases. In this review, we analyze some of the more recent findings regarding the study of brain aging and neurodegeneration in the context of mitophagy. We discuss the data on the dynamics of selective autophagy in neurons and glial cells during aging and in the course of neurodegeneration, focusing on three mechanisms of mitophagy: non-receptor-mediated mitophagy, receptor-mediated mitophagy, and transcellular mitophagy. We review the role of mitophagy in neuronal/glial homeostasis and in the molecular pathogenesis of neurodegenerative disorders, such as Parkinson’s disease, Alzheimer’s disease, and other disorders. Common mechanisms of aging and neurodegeneration that are related to different mitophagy pathways provide a number of promising targets for potential therapeutic agents.

scholarly journals Chronic administration of a positive allosteric modulator at the α5-GABAA receptor reverses age-related dendritic shrinkage

2020 ◽  
Author(s):  
Thomas D. Prevot ◽  
Akiko Sumitomo ◽  
Toshifumi Tomoda ◽  
Daniel E. Knutson ◽  
Guanguan Li ◽  
...  
Keyword(s):  
Life Expectancy ◽  
Cognitive Decline ◽  
Neuronal Morphology ◽  
Aging Brain ◽  
Primary Neuronal Culture ◽  
Efficient Treatment ◽  
Gaba A ◽  
Age Related ◽  
Β Amyloid ◽  
The Brain

ABSTRACTOver the last 15 years, worldwide life expectancy increased by 5 years jumping from 66 years to 71 years. With progress in science, medicine, and care we tend to live longer. Such extended life expectancy is still associated with age-related changes, including in the brain. The aging brain goes through various changes that can be called morphomolecular senescence. Overall, the brain volume changes, neuronal activity is modified and plasticity of the cells diminishes, sometimes leading to neuronal atrophy and death. Altogether, these changes contribute to the emergence of cognitive decline that still does not have an efficient treatment available. Many studies in the context of cognitive decline focused on pathological aging, targeting β-amyloid in Alzheimer’s disease, for example. However, β-amyloid plaques are also present in healthy adults and treatments targeting plaques have failed to improve cognitive functions. In order to improve the quality of life of aging population, it is crucial to focus on the development of novel therapies targeting different systems altered during aging, such as the GABAergic system. In previous studies, it has been shown that positive allosteric modulators (PAM) acting at the α5-containing GABA-A receptors improve cognitive performances, and that these α5-GABA-A receptors are implicated in dendritic growth of pyramidal neurons. Here, we hypothesized that targeting the α5-GABA-A receptors could contribute to the reduction of cognitive decline, directly through activity of the receptors, and indirectly by increasing neuronal morphology. Using primary neuronal culture and chronic treatment in mice, we demonstrated that an α5-PAM increased dendritic length, spine count and spine density in brain regions involved in cognitive processes (prefrontal cortex and hippocampus). We also confirmed the procognitive efficacy of the α5-PAM and showed that the washout period diminishes the precognitive effects without altering the effect on neuronal morphology. Future studies will be needed to investigate what downstream mechanisms responsible for the neurotrophic effect of the α5-PAM.

scholarly journals Bacopa monnierias an Antioxidant Therapy to Reduce Oxidative Stress in the Aging Brain

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Tamara Simpson ◽  
Matthew Pase ◽  
Con Stough
Keyword(s):  
Oxidative Stress ◽  
Cognitive Function ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Bacopa Monnieri ◽  
Aging Brain ◽  
Resonance Spectroscopy ◽  
Age Related

The detrimental effect of neuronal cell death due to oxidative stress and mitochondrial dysfunction has been implicated in age-related cognitive decline and neurodegenerative disorders such as Alzheimer’s disease. The Indian herbBacopa monnieriis a dietary antioxidant, with animal andin vitrostudies indicating several modes of action that may protect the brain against oxidative damage. In parallel, several studies using the CDRI08 extract have shown that extracts ofBacopa monnieriimprove cognitive function in humans. The biological mechanisms of this cognitive enhancement are unknown. In this review we discuss the animal studies andin vivoevidence forBacopa monnierias a potential therapeutic antioxidant to reduce oxidative stress and improve cognitive function. We suggest that future studies incorporate neuroimaging particularly magnetic resonance spectroscopy into their randomized controlled trials to better understand whether changes in antioxidant statusin vivocause improvements in cognitive function.

scholarly journals Age-related losses of cognitive function and motor skills in mice are associated with oxidative protein damage in the brain.

1996 ◽  
Vol 93 (10) ◽  
pp. 4765-4769 ◽  
Author(s):  
M. J. Forster ◽  
A. Dubey ◽  
K. M. Dawson ◽  
W. A. Stutts ◽  
H. Lal ◽  
...  
Keyword(s):  
Cognitive Function ◽  
Motor Skills ◽  
Protein Damage ◽  
Age Related ◽  
Oxidative Protein Damage ◽  
The Brain

N-acetyl-l-cysteine attenuates oxidative damage and neurodegeneration in rat brain during aging

2018 ◽  
Vol 96 (12) ◽  
pp. 1189-1196 ◽  
Author(s):  
Geetika Garg ◽  
Sandeep Singh ◽  
Abhishek Kumar Singh ◽  
Syed Ibrahim Rizvi
Keyword(s):  
Rat Brain ◽  
Neuroprotective Effect ◽  
Neuron Specific Enolase ◽  
Sirtuin 1 ◽  
Marker Genes ◽  
Aging Brain ◽  
Age Related ◽  
Nonenzymatic Antioxidants ◽  
Old Rats ◽  
The Brain

N-acetyl-l-cysteine (NAC) is a precursor of cysteine, which is known to increase the level of glutathione (GSH) in the brain. Several neurodegenerative changes linked to oxidative stress take place in the aging brain. This study aimed to assess the neuroprotective effect of NAC supplementation on age-dependent neurodegeneration in the rat brain. Young (4 months) and old (24 months) Wistar rats (n = 6 rats/group) were supplemented with NAC (100 mg/kg b.w. orally) for 14 days. Enzymatic and nonenzymatic antioxidants such as superoxide dismutase and catalase, and GSH and total thiol respectively, prooxidants such as protein carbonyl, advanced oxidation protein products, reactive oxygen species, and malondialdehyde were assessed in the brain homogenates. Furthermore, nitric oxide level, acetylcholinesterase activity, and Na+/K+–ATPase activity were measured and gene expression studies were also performed. The results indicated that NAC augmented the level of enzymatic and nonenzymatic antioxidants with a significant reduction in prooxidant levels in old rats. NAC supplementation also downregulated the expression of inflammatory markers (TNF-α, IL-1β, IL-6) and upregulated the expression of marker genes associated with aging (sirtuin-1) and neurodegeneration (neuron-specific enolase, neuroglobin, synapsin-I, myelin basic protein 2) in old rats. The present findings support a neuroprotective role of NAC which has therapeutic implication in controlling age-related neurological disorders.

CORRELATION OF MORNING SALIVARY CORTISOL-MELATONIN RATIO WITH QEEG AND DELAYED RECALL IN AGING

2018 ◽  
Vol 16 (2) ◽  
pp. 177-188
Author(s):  
Watchara Sroykham ◽  
Yodchanan Wongsawat
Keyword(s):  
Circadian Rhythm ◽  
Cognitive Function ◽  
Temporal Lobe ◽  
Brain Activity ◽  
High Ratio ◽  
Left Temporal Lobe ◽  
Delayed Recall ◽  
Age Related ◽  
Eyes Open ◽  
The Brain

Melatonin and cortisol are the main hormones of the circadian rhythm, which effect cognitive decline during aging. An imbalance of circadian rhythm hormones serves as an early sign of the progress of age-related disease and brain pathology in aging. The aim of this study was to determine the cortisol-melatonin ratio in relation to brain activity and cognitive function in aging. Sixty-four aging subjects were recruited from the brain healthy project. The morning salivary of all subjects was collected for cortisol and melatonin levels analysis. The brain activity was recorded for 5 minutes in the eyes open condition and seven cognitive functions were assessed by the MoCA. The results were divided into a low ratio group and a high ratio group of cortisol-melatonin ratio. The low ratio group and the high ratio group differed in the delta-beta ratio at the left temporal lope (p < .05), and the delayed recall in the high ratio group was markedly higher than in the low ratio group. Moreover, the cortisol-melatonin ratio was strongly correlated with delayed recall (p < .05), the delta-beta ratio in the left temporal lope (p <.05), the theta alpha ratio in the left temporal lope (p < .05), and right temporal lope (p < .05). We found that a low cortisol-melatonin ratio corresponded to a high delta-beta ratio and a high thetaalpha ratio at the left temporal lobe with a low score of delayed recall function, but a high cortisol-melatonin ratio corresponded to a low delta-beta ratio and a low theta-alpha ratio at the left temporal lobe with a high score of delayed recall. The imbalance of the circadian hormone related to cognitive function and brain activity in aging could serve as a biomarker of age-related diseases.

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