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Neuroplasticity and brain change

The brain changing with experience and practice.

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المكتبة البحثية677 works held

Peer-reviewed work held with its DOI and abstract, labelled with the study design its publication types report. None of it has been read or assessed, so nothing here may be cited as showing anything. Retracted work is held for the record but never listed; a review that a later version replaced is listed under its replacement and marked.

10.2165/11595900-000000000-00000CNS drugs (2011)MEDLINE-indexed journal, not yet read by us; matched on Neuronal Plasticity, Brain-Derived Neurotrophic Factor, Neurogenesis, synaptic plasticity, Hippocampus

The hippocampus, neurotrophic factors and depression: possible implications for the pharmacotherapy of depression.: Depression is a prevalent, highly debilitating mental disorder affecting up to 15% of the population at least once in their lifetime, with huge costs for society. Neurobiological mechanisms of depression are still not well known, although there is consensus about interplay between genetic and environmental factors. Antidepressant medications are frequently used in depression, but at least 50% of patients are poor responders, even to more recently discovered medications. Furthermore, clinical res

10.1111/j.1748-1716.2009.02021.xActa physiologica (Oxford, England) (2010)MEDLINE-indexed journal, not yet read by us; matched on Neuronal Plasticity, Long-Term Potentiation, synaptic plasticity, Hippocampus, Synapses

Orexins/hypocretins control bistability of hippocampal long-term synaptic plasticity through co-activation of multiple kinases.: Aim: Orexins/hypocretins (OX/Hcrt) are hypothalamic neuropeptides linking sleep-wakefulness, appetite and neuroendocrine control. Their role and mechanisms of action on higher brain functions, such as learning and memory, are not clear. Methods: We used field recordings of excitatory post-synaptic potentials (fEPSP) in acute mouse brain slice preparations to study the effects of orexins and pharmacological inhibitors of multiple kinases on long-term synaptic plasticity in the hippocampus. Result

10.1016/j.amepre.2011.10.016American journal of preventive medicine (2012)MEDLINE-indexed journal, not yet read by us; matched on Neuronal Plasticity, Brain-Derived Neurotrophic Factor, neuroplasticity

Exergaming and older adult cognition: a cluster randomized clinical trial.: Background: Dementia cases may reach 100 million by 2050. Interventions are sought to curb or prevent cognitive decline. Exercise yields cognitive benefits, but few older adults exercise. Virtual reality-enhanced exercise or "exergames" may elicit greater participation. Purpose: To test the following hypotheses: (1) stationary cycling with virtual reality tours ("cybercycle") will enhance executive function and clinical status more than traditional exercise; (2) exercise effort will explain impr

10.1016/j.biopsych.2009.03.022Biological psychiatry (2009)MEDLINE-indexed journal, not yet read by us; matched on Neuronal Plasticity, Evoked Potentials, Motor, neuroplasticity, Motor Cortex

Serotonin affects transcranial direct current-induced neuroplasticity in humans.: Background: Modulation of the serotonergic system affects long-term potentiation (LTP) and long-term depression (LTD), the likely neurophysiologic derivates of learning and memory formation, in animals and slice preparations. Serotonin-dependent modulation of plasticity has been proposed as an underlying mechanism for depression. However, direct knowledge about the impact of serotonin on neuroplasticity in humans is missing. Here we explore the impact of the serotonin reuptake blocker citalopram

10.1017/s1461145708009309The international journal of neuropsychopharmacology (2008)MEDLINE-indexed journal, not yet read by us; matched on Neuronal Plasticity, Brain-Derived Neurotrophic Factor, neuroplasticity

A systematic review and meta-analysis of clinical studies on major depression and BDNF levels: implications for the role of neuroplasticity in depression.: Several clinical studies on major depressive disorder (MDD) have shown that blood brain-derived neurotrophic factor (BDNF) - a factor used to index neuroplasticity - is associated with depression response; however, the results are mixed. The purpose of our study was to evaluate whether BDNF levels are correlated with improvement of depression. We performed a systematic review and meta-analysis of the literature, searching Medline, Cochrane Central, SciELO databases and reference lists from retri

10.2165/11534530-000000000-00000Sports medicine (Auckland, N.Z.) (2010)MEDLINE-indexed journal, not yet read by us; matched on Neuronal Plasticity, Brain-Derived Neurotrophic Factor, neuroplasticity

Neuroplasticity - exercise-induced response of peripheral brain-derived neurotrophic factor: a systematic review of experimental studies in human subjects.: Exercise is known to induce a cascade of molecular and cellular processes that support brain plasticity. Brain-derived neurotrophic factor (BDNF) is an essential neurotrophin that is also intimately connected with central and peripheral molecular processes of energy metabolism and homeostasis, and could play a crucial role in these induced mechanisms. This review provides an overview of the current knowledge on the effects of acute exercise and/or training on BDNF in healthy subjects and in pers

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Goh JO, Park DC (2009)reviewMEDLINE-indexed journal, not yet read by usRestorative neurology and neuroscience156 citations

Neuroplasticity and cognitive aging: the scaffolding theory of aging and cognition.

A recent proposal called the Scaffolding Theory of Cognitive Aging (STAC) postulates that functional changes with aging are part of a lifespan process of compensatory cognitive scaffolding that is an attempt to alleviate the cognitive declines associated with aging. Indeed, behavioral studies have shown that aging is associated with both decline as well as preservation of selective cognitive abilities. Similarly, neuroimaging studies have revealed selective changes in the aging brain that reflect neural decline as well as compensatory neural recruitment. While aging is associated with reductions in cortical thickness, white-matter integrity, dopaminergic activity, and functional engagement in posterior brain regions such as the hippocampus and occipital areas, there are compensatory increases in frontal functional engagement that correlate with better behavioral performance in older adul

matched on Neuronal Plasticity (mesh), neuroplasticity (text), Synapses (mesh)

Murphy TH, Corbett D (2009)reviewMEDLINE-indexed journal, not yet read by usNature reviews. Neuroscience1,337 citations

Plasticity during stroke recovery: from synapse to behaviour.

Reductions in blood flow to the brain of sufficient duration and extent lead to stroke, which results in damage to neuronal networks and the impairment of sensation, movement or cognition. Evidence from animal models suggests that a time-limited window of neuroplasticity opens following a stroke, during which the greatest gains in recovery occur. Plasticity mechanisms include activity-dependent rewiring and synapse strengthening. The challenge for improving stroke recovery is to understand how to optimally engage and modify surviving neuronal networks, to provide new response strategies that compensate for tissue lost to injury.

matched on Neuronal Plasticity (mesh), neuroplasticity (text), Synapses (mesh)

Petrosini L, De Bartolo P, Foti F, Gelfo F, Cutuli D, Leggio MG, Mandolesi L (2009)reviewMEDLINE-indexed journal, not yet read by usBrain research reviews154 citations

On whether the environmental enrichment may provide cognitive and brain reserves.

The construct of brain and cognitive reserves holds that cognitive enrichment fosters the development of neuroplasticity properties, which permit normal cognitive functioning even in the presence of brain pathology. Interpreting the experience-dependent increase of neuronal connectivity and efficiency in the light of the reserve theory provides an interesting approach for explaining the maintenance of cognitive function observed in some subjects affected by neurodegenerative disorders. In fact, mental and physical engagement with complex environments strengthens synaptic connectivity and provides the means by which preexisting neuronal networks are efficiently utilized and alternative networks are recruited to meet environmental demands and to cope with brain damage. There is considerable interest in determining the biological factors that allow the development of these reserves. To inve

matched on Neuronal Plasticity (mesh), neuroplasticity (text), Synapses (mesh)

Fontán-Lozano A, López-Lluch G, Delgado-García JM, Navas P, Carrión AM (2008)reviewMEDLINE-indexed journal, not yet read by usMolecular neurobiology67 citations

Molecular bases of caloric restriction regulation of neuronal synaptic plasticity.

Aging is associated with the decline of cognitive properties. This situation is magnified when neurodegenerative processes associated with aging appear in human patients. Neuronal synaptic plasticity events underlie cognitive properties in the central nervous system. Caloric restriction (CR; either a decrease in food intake or an intermittent fasting diet) can extend life span and increase disease resistance. Recent studies have shown that CR can have profound effects on brain function and vulnerability to injury and disease. Moreover, CR can stimulate the production of new neurons from stem cells (neurogenesis) and can enhance synaptic plasticity, which modulate pain sensation, enhance cognitive function, and may increase the ability of the brain to resist aging. The beneficial effects of CR appear to be the result of a cellular stress response stimulating the production of proteins tha

matched on Neuronal Plasticity (mesh), synaptic plasticity (text), Synapses (mesh)

Calabresi P, Picconi B, Tozzi A, Di Filippo M (2007)reviewMEDLINE-indexed journal, not yet read by usTrends in neurosciences628 citations

Dopamine-mediated regulation of corticostriatal synaptic plasticity.

The striatum represents the main input into the basal ganglia. Neurons projecting from the striatum receive a large convergence of afferents from all areas of the cortex and transmit neural information to the basal ganglia output structures. Corticostriatal transmission is essential in the regulation of voluntary movement, in addition to behavioural control, cognitive function and reward mechanisms. Long-term potentiation (LTP) and long-term depression (LTD), the two main forms of synaptic plasticity, are both represented at corticostriatal synapses and strongly depend on the activation of dopamine receptors. Here, we discuss possible feedforward and feedback mechanisms by which striatal interneurons, in association with striatal spiny neurons and endogenous dopamine, influence the formation and maintenance of both LTP and LTD. We also propose a model in which the spontaneous membrane os

matched on Neuronal Plasticity (mesh), synaptic plasticity (text), Synapses (mesh)

Rosanova M, Ulrich D (2005)cohort or longitudinalMEDLINE-indexed journal, not yet read by usThe Journal of neuroscience : the official journal of the Society for Neuroscience315 citations

Pattern-specific associative long-term potentiation induced by a sleep spindle-related spike train.

Spindles are non-rapid eye movement (non-REM) sleep EEG rhythms (7-14 Hz) that occur independently or in association with slow oscillations (0.6-0.8 Hz). Despite their proposed function in learning and memory, their role in synaptic plasticity is essentially unknown. We studied the ability of a neuronal firing pattern underlying spindles in vivo to induce synaptic plasticity in neocortical pyramidal cells in vitro. A spindle stimulation pattern (SSP) was extracted from a slow oscillation upstate that was recorded in a cat anesthetized with ketamine-xylazine, which is known to induce a sleep-like state. To mimic the recurrence of spindles grouped by the slow oscillation, the SSP was repeated every 1.5 s (0.6 Hz). Whole-cell patch-clamp recordings were obtained from layer V pyramidal cells of rat somatosensory cortex with infrared videomicroscopy, and composite EPSPs were evoked within lay

matched on Long-Term Potentiation (mesh), synaptic plasticity (text)

Premoli I, Rivolta D, Espenhahn S, Castellanos N, Belardinelli P, Ziemann U, Müller-Dahlhaus F (2014)randomised controlled trialMEDLINE-indexed journal, not yet read by usNeuroImage133 citations

Characterization of GABAB-receptor mediated neurotransmission in the human cortex by paired-pulse TMS-EEG.

GABAB-receptor (GABABR) mediated inhibition is important in regulating neuronal excitability. The paired-pulse transcranial magnetic stimulation (TMS) protocol of long-interval intracortical inhibition (LICI) likely reflects this GABABergic inhibition. However, this view is based on indirect evidence from electromyographic (EMG) studies. Here we combined paired-pulse TMS with simultaneous electroencephalography (paired-pulse TMS-EEG) and pharmacology to directly investigate mechanisms of LICI at the cortical level. We tested the effects of a conditioning stimulus (CS100) applied 100ms prior to a test stimulus (TS) over primary motor cortex on TS-evoked EEG-potentials (TEPs). Healthy subjects were given a single oral dose of baclofen, a GABABR agonist, or diazepam, a positive modulator at GABAARs, in a placebo-controlled, pseudo-randomized double-blinded crossover study. LICI was quantifi

matched on Evoked Potentials, Motor (mesh)

George MS, Lisanby SH, Avery D, McDonald WM, Durkalski V, Pavlicova M, Anderson B, Nahas Z, Bulow P, Zarkowski P, Holtzheimer PE, Schwartz T, Sackeim HA (2010)randomised controlled trialMEDLINE-indexed journal, not yet read by usArchives of general psychiatry753 citations

Daily left prefrontal transcranial magnetic stimulation therapy for major depressive disorder: a sham-controlled randomized trial.

Context: Daily left prefrontal repetitive transcranial magnetic stimulation (rTMS) has been studied as a potential treatment for depression, but previous work had mixed outcomes and did not adequately mask sham conditions. Objective: To test whether daily left prefrontal rTMS safely and effectively treats major depressive disorder. Design: Prospective, multisite, randomized, active sham-controlled (1:1 randomization), duration-adaptive design with 3 weeks of daily weekday treatment (fixed-dose phase) followed by continued blinded treatment for up to another 3 weeks in improvers. Setting: Four US university hospital clinics. Patients: Approximately 860 outpatients were screened, yielding 199 antidepressant drug-free patients with unipolar nonpsychotic major depressive disorder. Intervention: We delivered rTMS to the left prefrontal cortex at 120% motor threshold (10 Hz, 4-second train dur

matched on Evoked Potentials, Motor (mesh)

Zhang JC, Lau PM, Bi GQ (2009)MEDLINE-indexed journal, not yet read by usProceedings of the National Academy of Sciences of the United States of America139 citations

Gain in sensitivity and loss in temporal contrast of STDP by dopaminergic modulation at hippocampal synapses.

Spike-timing-dependent plasticity (STDP) is considered a physiologically relevant form of Hebbian learning. However, behavioral learning often involves action of reinforcement or reward signals such as dopamine. Here, we examined how dopamine influences the quantitative rule of STDP at glutamatergic synapses of hippocampal neurons. The presence of 20 muM dopamine during paired pre- and postsynaptic spiking activity expanded the effective time window for timing-dependent long-term potentiation (t-LTP) to at least -45 ms, and allowed normally ineffective weak stimuli with fewer spike pairs to induce significant t-LTP. Meanwhile, dopamine did not affect the degree of t-LTP induced by normal strong stimuli with spike timing (ST) of +10 ms. Such dopamine-dependent enhancement in the sensitivity of t-LTP was completely blocked by the D1-like dopamine receptor antagonist SCH23390, but not by th

matched on Neuronal Plasticity (mesh), Long-Term Potentiation (mesh), Hippocampus (mesh), Receptors, N-Methyl-D-Aspartate (mesh), Synapses (mesh)

Eschenko O, Mölle M, Born J, Sara SJ (2006)cohort or longitudinalMEDLINE-indexed journal, not yet read by usThe Journal of neuroscience : the official journal of the Society for Neuroscience197 citations

Elevated sleep spindle density after learning or after retrieval in rats.

Non-rapid eye movement sleep has been strongly implicated in consolidation of both declarative and procedural memory in humans. Elevated sleep-spindle density in slow-wave sleep after learning has been shown recently in humans. It has been proposed that sleep spindles, 12-15 Hz oscillations superimposed on slow waves (<1 Hz), in concert with high-frequency hippocampal sharp waves/ripples, promote neural plasticity underlying remote memory formation. The present study reports the first indication of learning-associated increase in spindle density in the rat, providing an animal model to study the role of brain oscillations in memory consolidation during sleep. An odor-reward association task, analogous in many respects to human paired-associate learning, is rapidly learned and leads to robust memory in rats. Rats learned the task over 10 massed trials within a single session, and EEG was

matched on Neuronal Plasticity (mesh)

Hernandez PJ, Schiltz CA, Kelley AE (2006)cohort or longitudinalMEDLINE-indexed journal, not yet read by usLearning & memory (Cold Spring Harbor, N.Y.)39 citations

Dynamic shifts in corticostriatal expression patterns of the immediate early genes Homer 1a and Zif268 during early and late phases of instrumental training.

Adaptive motor actions require prior knowledge of instrumental contingencies. With practice, these actions can become highly automatic in nature. However, the molecular and anatomical substrates mediating these related forms of learning are not understood. In the present study, we used in situ hybridization to measure the mRNA levels of two immediate early genes (IEGs) in an instrumental paradigm where rats learned to lever-press for food. We report that after three training sessions, Homer 1a and Zif268 (an effector and regulatory IEG, respectively) were significantly induced within an extensive corticostriatal network relative to untrained controls. With extended training (23 sessions), however, a shift in the expression patterns of the two genes was evident. Expression of Homer 1a (official symbol Homer1) decreased significantly in frontal and cingulate cortices, whereas striatal expr

matched on Neuronal Plasticity (mesh)

Walker MP, Stickgold R, Alsop D, Gaab N, Schlaug G (2005)cohort or longitudinalMEDLINE-indexed journal, not yet read by usNeuroscience203 citations

Sleep-dependent motor memory plasticity in the human brain.

Growing evidence indicates a role for sleep in off-line memory processing, specifically in post-training consolidation. In humans, sleep has been shown to trigger overnight learning on a motor-sequence memory task, while equivalent waking periods produce no such improvement. But while the behavioral characteristics of sleep-dependent motor learning become increasingly well characterized, the underlying neural basis remains unknown. Here we present functional magnetic resonance imaging data demonstrating a change in the representation of a motor memory after a night of sleep. Subjects trained on a motor-skill memory and 12 hours later, after either sleep or wake, were retested during functional magnetic resonance imaging. Following sleep relative to wake, regions of increased activation were expressed in the right primary motor cortex, medial prefrontal lobe, hippocampus and left cerebell

matched on Neuronal Plasticity (mesh)

Beilharz JE, Maniam J, Morris MJ (2015)reviewMEDLINE-indexed journal, not yet read by usNutrients150 citations

Diet-Induced Cognitive Deficits: The Role of Fat and Sugar, Potential Mechanisms and Nutritional Interventions.

It is of vital importance to understand how the foods which are making us fat also act to impair cognition. In this review, we compare the effects of acute and chronic exposure to high-energy diets on cognition and examine the relative contributions of fat (saturated and polyunsaturated) and sugar to these deficits. Hippocampal-dependent memory appears to be particularly vulnerable to the effects of high-energy diets and these deficits can occur rapidly and prior to weight gain. More chronic diet exposure seems necessary however to impair other sorts of memory. Many potential mechanisms have been proposed to underlie diet-induced cognitive decline and we will focus on inflammation and the neurotrophic factor, brain-derived neurotrophic factor (BDNF). Finally, given supplementation of diets with omega-3 and curcumin has been shown to have positive effects on cognitive function in healthy

matched on Brain-Derived Neurotrophic Factor (mesh), Neurogenesis (keyword), Hippocampus (mesh)

Kandola A, Ashdown-Franks G, Hendrikse J, Sabiston CM, Stubbs B (2019)reviewMEDLINE-indexed journal, not yet read by usNeuroscience and biobehavioral reviews830 citations

Physical activity and depression: Towards understanding the antidepressant mechanisms of physical activity.

Physical activity can treat and prevent depressive symptoms, but its antidepressant mechanisms are yet to be established. In this review, we comprehensively assess key biological and psychosocial mechanisms through which physical activity exerts antidepressant effects, with a particular focus on exercise. Exercise, a subset of physical activity, influences a range of biological and psychosocial processes also implicated in the pathophysiology of depression. We focus on the capacity for exercise to elicit changes in neuroplasticity, inflammation, oxidative stress, the endocrine system, self-esteem, social support and self-efficacy. We also discuss how a better understanding of these mechanisms can inform the way we design and implement exercise-based interventions to maximise their antidepressant effects on an individual basis. We conclude by presenting a conceptual framework of the key b

matched on Neuronal Plasticity (mesh), neuroplasticity (text), Hippocampus (keyword)

Mattson MP, Arumugam TV (2018)reviewMEDLINE-indexed journal, not yet read by usCell metabolism931 citations

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

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.

matched on Neuronal Plasticity (mesh), neuroplasticity (text), Hippocampus (keyword)

Katusic ZS, Austin SA (2014)reviewMEDLINE-indexed journal, not yet read by usEuropean heart journal173 citations

Endothelial nitric oxide: protector of a healthy mind.

Endothelial nitric oxide (NO) is generated by constitutively active endothelial nitric oxide synthase (eNOS), an essential enzyme responsible for cardiovascular homeostasis. Historically, endothelial NO was first recognized as a major vasodilator involved in control of vasomotor function and local blood flow. In this review, our attention is focused on the emerging role of endothelial NO in linking cerebrovascular function with cognition. We will discuss the recognized ability of endothelial NO to modulate processing of amyloid precursor protein (APP), influence functional status of microglia, and affect cognitive function. Existing evidence suggests that the loss of NO in cultured human cerebrovascular endothelium causes increased expression of APP and β-site APP-cleaving enzyme 1 (BACE1) thereby resulting in increased secretion of amyloid β peptides (Aβ1-40 and Aβ1-42). Furthermore, in

matched on Neuronal Plasticity (mesh), synaptic plasticity (text), Hippocampus (keyword)

Morris GP, Clark IA, Zinn R, Vissel B (2013)reviewMEDLINE-indexed journal, not yet read by usNeurobiology of learning and memory175 citations

Microglia: a new frontier for synaptic plasticity, learning and memory, and neurodegenerative disease research.

We focus on emerging roles for microglia in synaptic plasticity, cognition and disease. We outline evidence that ramified microglia, traditionally thought to be functionally "resting" (i.e. quiescent) in the normal brain, in fact are highly dynamic and plastic. Ramified microglia continually and rapidly extend processes, contact synapses in an activity and experience dependent manner, and play a functionally dynamic role in synaptic plasticity, possibly through release of cytokines and growth factors. Ramified microglial also contribute to structural plasticity through the elimination of synapses via phagocytic mechanisms, which is necessary for normal cognition. Microglia have numerous mechanisms to monitor neuronal activity and numerous mechanisms also exist to prevent them transitioning to an activated state, which involves retraction of their surveying processes. Based on the evidenc

matched on Neuronal Plasticity (mesh), synaptic plasticity (text), Synapses (keyword)

Gordon PC, Desideri D, Belardinelli P, Zrenner C, Ziemann U (2018)cohort or longitudinalMEDLINE-indexed journal, not yet read by usBrain stimulation100 citations

Comparison of cortical EEG responses to realistic sham versus real TMS of human motor cortex.

Background: The analysis of cortical responses to transcranial magnetic stimulation (TMS) recorded by electroencephalography (EEG) has been successfully applied to study human cortical physiology. However, in addition to the (desired) activation of cortical neurons and fibers, TMS also causes (undesired) indirect brain responses through auditory and somatosensory stimulation, which may contribute significantly to the overall EEG signal and mask the effects of intervention on direct cortical responses. Objectives: To test differences in EEG responses to real TMS at intensities above and below resting motor threshold (RMT) and a realistic sham stimulation. Methods: 12 healthy subjects participated in one session in which single-pulse TMS was applied to the left motor cortex in 3 different blocks, 150 pulses per block: 110%RMT, 90%RMT and realistic sham stimulation. Cortical responses were

matched on Evoked Potentials, Motor (mesh), Motor Cortex (mesh), Motor Cortex (keyword)

Mahalakshmi B, Maurya N, Lee SD, Bharath Kumar V (2020)reviewMEDLINE-indexed journal, not yet read by usInternational journal of molecular sciences230 citations

Possible Neuroprotective Mechanisms of Physical Exercise in Neurodegeneration.

Physical exercise (PE) improves physical performance, mental status, general health, and well-being. It does so by affecting many mechanisms at the cellular and molecular level. PE is beneficial for people suffering from neuro-degenerative diseases because it improves the production of neurotrophic factors, neurotransmitters, and hormones. PE promotes neuronal survival and neuroplasticity and also optimizes neuroendocrine and physiological responses to psychosocial and physical stress. PE sensitizes the parasympathetic nervous system (PNS), Autonomic Nervous System (ANS) and central nervous system (CNS) by promoting many processes such as synaptic plasticity, neurogenesis, angiogenesis, and autophagy. Overall, it carries out many protective and preventive activities such as improvements in memory, cognition, sleep and mood; growth of new blood vessels in nervous system; and the reduction

matched on Brain-Derived Neurotrophic Factor (mesh), neuroplasticity (text), synaptic plasticity (text)

Petzinger GM, Fisher BE, McEwen S, Beeler JA, Walsh JP, Jakowec MW (2013)MEDLINE-indexed journal, not yet read by usThe Lancet. Neurology543 citations

Exercise-enhanced neuroplasticity targeting motor and cognitive circuitry in Parkinson's disease.

Exercise interventions in individuals with Parkinson's disease incorporate goal-based motor skill training to engage cognitive circuitry important in motor learning. With this exercise approach, physical therapy helps with learning through instruction and feedback (reinforcement) and encouragement to perform beyond self-perceived capability. Individuals with Parkinson's disease become more cognitively engaged with the practice and learning of movements and skills that were previously automatic and unconscious. Aerobic exercise, regarded as important for improvement of blood flow and facilitation of neuroplasticity in elderly people, might also have a role in improvement of behavioural function in individuals with Parkinson's disease. Exercises that incorporate goal-based training and aerobic activity have the potential to improve both cognitive and automatic components of motor control i

matched on Neuronal Plasticity (mesh), Neurogenesis (mesh), Dendritic Spines (mesh), neuroplasticity (text)

Ho N, Sommers MS, Lucki I (2013)reviewMEDLINE-indexed journal, not yet read by usNeuroscience and biobehavioral reviews199 citations

Effects of diabetes on hippocampal neurogenesis: links to cognition and depression.

Diabetes often leads to a number of complications involving brain function, including cognitive decline and depression. In addition, depression is a risk factor for developing diabetes. A loss of hippocampal neuroplasticity, which impairs the ability of the brain to adapt and reorganize key behavioral and emotional functions, provides a framework for understanding this reciprocal relationship. The effects of diabetes on brain and behavioral functions in experimental models of type 1 and type 2 diabetes are reviewed, with a focus on the negative impact of impaired hippocampal neurogenesis, dendritic remodeling and increased apoptosis. Mechanisms shown to regulate neuroplasticity and behavior in diabetes models, including stress hormones, neurotransmitters, neurotrophins, inflammation and aging, are integrated within this framework. Pathological changes in hippocampal function can contribu

matched on Neurogenesis (mesh), neuroplasticity (text), Hippocampus (mesh)

Mang CS, Snow NJ, Campbell KL, Ross CJ, Boyd LA (2014)MEDLINE-indexed journal, not yet read by usJournal of applied physiology (Bethesda, Md. : 1985)164 citations

A single bout of high-intensity aerobic exercise facilitates response to paired associative stimulation and promotes sequence-specific implicit motor learning.

The objectives of the present study were to evaluate the impact of a single bout of high-intensity aerobic exercise on 1) long-term potentiation (LTP)-like neuroplasticity via response to paired associative stimulation (PAS) and 2) the temporal and spatial components of sequence-specific implicit motor learning. Additionally, relationships between exercise-induced increases in systemic brain-derived neurotrophic factor (BDNF) and response to PAS and motor learning were evaluated. Sixteen young healthy participants completed six experimental sessions, including the following: 1) rest followed by PAS; 2) aerobic exercise followed by PAS; 3) rest followed by practice of a continuous tracking (CT) task and 4) a no-exercise 24-h retention test; and 5) aerobic exercise followed by CT task practice and 6) a no-exercise 24-h retention test. The CT task included an embedded repeated sequence allo

matched on Neuronal Plasticity (mesh), Brain-Derived Neurotrophic Factor (mesh), Brain-Derived Neurotrophic Factor (keyword), neuroplasticity (text)

Podda MV, Cocco S, Mastrodonato A, Fusco S, Leone L, Barbati SA, Colussi C, Ripoli C, Grassi C (2016)MEDLINE-indexed journal, not yet read by usScientific reports174 citations

Anodal transcranial direct current stimulation boosts synaptic plasticity and memory in mice via epigenetic regulation of Bdnf expression.

The effects of transcranial direct current stimulation (tDCS) on brain functions and the underlying molecular mechanisms are yet largely unknown. Here we report that mice subjected to 20-min anodal tDCS exhibited one-week lasting increases in hippocampal LTP, learning and memory. These effects were associated with enhanced: i) acetylation of brain-derived neurotrophic factor (Bdnf) promoter I; ii) expression of Bdnf exons I and IX; iii) Bdnf protein levels. The hippocampi of stimulated mice also exhibited enhanced CREB phosphorylation, pCREB binding to Bdnf promoter I and recruitment of CBP on the same regulatory sequence. Inhibition of acetylation and blockade of TrkB receptors hindered tDCS effects at molecular, electrophysiological and behavioral levels. Collectively, our findings suggest that anodal tDCS increases hippocampal LTP and memory via chromatin remodeling of Bdnf regulatory

matched on Brain-Derived Neurotrophic Factor (mesh), Long-Term Potentiation (mesh), neuroplasticity (text), synaptic plasticity (text), Hippocampus (mesh)

Brain-derived neurotrophic factor (BDNF) gene polymorphisms shape cortical plasticity in humans.

Background: The brain-derived neurotrophic factor (BDNF) gene is involved in mechanisms of synaptic plasticity in the adult brain. It has been demonstrated that BDNF also plays a significant role in shaping externally induced human brain plasticity. Plasticity induced in the human motor cortex by intermittent theta-burst stimulation (iTBS) was impaired in individuals expressing the Val66Met polymorphism. Methods: To explore whether this polymorphism is also important for other neuroplasticity-inducing tools in humans with modes of action differing from that of iTBS, namely, transcranial direct current (tDCS) and random noise stimulation (tRNS), we retrospectively analyzed the data of 64 subjects studied in our laboratory with regard to BDNF genotype. Results: Fifteen subjects with the Val66Met allele, 46 subjects with the Val66Val allele, and 3 Met66Met carriers were identified. The resp

matched on Neuronal Plasticity (mesh), Brain-Derived Neurotrophic Factor (mesh), neuroplasticity (text), synaptic plasticity (text)

Wu A, Ying Z, Gomez-Pinilla F (2008)MEDLINE-indexed journal, not yet read by usNeuroscience213 citations

Docosahexaenoic acid dietary supplementation enhances the effects of exercise on synaptic plasticity and cognition.

Omega-3 fatty acids (i.e. docosahexaenoic acid; DHA), similar to exercise, improve cognitive function, promote neuroplasticity, and protect against neurological lesion. In this study, we investigated a possible synergistic action between DHA dietary supplementation and voluntary exercise on modulating synaptic plasticity and cognition. Rats received DHA dietary supplementation (1.25% DHA) with or without voluntary exercise for 12 days. We found that the DHA-enriched diet significantly increased spatial learning ability, and these effects were enhanced by exercise. The DHA-enriched diet increased levels of pro-brain-derived neurotrophic factor (BDNF) and mature BDNF, whereas the additional application of exercise boosted the levels of both. Furthermore, the levels of the activated forms of CREB and synapsin I were incremented by the DHA-enriched diet with greater elevation by the concurre

matched on Neuronal Plasticity (mesh), Brain-Derived Neurotrophic Factor (mesh), neuroplasticity (text), synaptic plasticity (text)