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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

Research library, full list

451 to 475 of 677
Foley TE, Fleshner M (2008)MEDLINE-indexed journal, not yet read by usNeuromolecular medicine162 citations

Neuroplasticity of dopamine circuits after exercise: implications for central fatigue.

Habitual exercise increases plasticity in a variety of neurotransmitter systems. The current review focuses on the effects of habitual physical activity on monoamine dopamine (DA) neurotransmission and the potential implication of these changes to exercise-induced fatigue. Although it is clear that peripheral adaptations in muscle and energy substrate utilization contribute to this effect, more recently it has been suggested that central nervous system pathways "upstream" of the motor cortex, which initiate activation of skeletal muscles, are also important. The contribution of the brain to exercise-induced fatigue has been termed "central fatigue." Given the well-defined role of DA in the initiation of movement, it is likely that adaptations in DA systems influence exercise capacity. A reduction in DA neurotransmission in the substantia nigra pars compacta (SNpc), for example, could imp

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

Heuninckx S, Wenderoth N, Swinnen SP (2008)MEDLINE-indexed journal, not yet read by usThe Journal of neuroscience : the official journal of the Society for Neuroscience401 citations

Systems neuroplasticity in the aging brain: recruiting additional neural resources for successful motor performance in elderly persons.

Functional imaging studies have shown that seniors exhibit more elaborate brain activation than younger controls while performing motor tasks. Here, we investigated whether this age-related overactivation reflects compensation or dedifferentiation mechanisms. "Compensation" refers to additional activation that counteracts age-related decline of brain function and supports successful performance, whereas "dedifferentiation" reflects age-related difficulties in recruiting specialized neural mechanisms and is not relevant to task performance. To test these predictions, performance on a complex interlimb coordination task was correlated with brain activation. Findings revealed that coordination resulted in activation of classical motor coordination regions, but also higher-level sensorimotor regions, and frontal regions in the elderly. Interestingly, a positive correlation between activation

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

Ding DC, Shyu WC, Chiang MF, Lin SZ, Chang YC, Wang HJ, Su CY, Li H (2007)MEDLINE-indexed journal, not yet read by usNeurobiology of disease160 citations

Enhancement of neuroplasticity through upregulation of beta1-integrin in human umbilical cord-derived stromal cell implanted stroke model.

Neuroplasticity subsequent to functional angiogenesis is an important goal for cell-based therapy of ischemic neural tissues. At present, the cellular and molecular mechanisms involved are still not well understood. In this study, we isolated mesenchymal stem cells (MSCs) from Wharton's jelly (WJ) to obtain clonally expanded human umbilical cord-derived mesenchymal stem cells (HUCMSCs) with multilineage differentiation potential. Experimental rats receiving intracerebral HUCMSC transplantation showed significantly improved neurological function compared to vehicle-treated control rats. Cortical neuronal activity, as evaluated by proton MR spectroscopy (1H-MRS), also increased considerably in the transplantation group. Transplanted HUCMSCs migrated towards the ischemic boundary zone and differentiated into glial, neuronal, doublecortin+, CXCR4+, and vascular endothelial cells to enhance n

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

Zuo Y, Smith DC, Jensen RA (2007)MEDLINE-indexed journal, not yet read by usPhysiology & behavior112 citations

Vagus nerve stimulation potentiates hippocampal LTP in freely-moving rats.

Previous studies have demonstrated that electrical stimulation of the vagus nerve (VNS) delivered at a moderate intensity following a learning experience enhances memory in laboratory rats and human subjects, while VNS at lower or higher intensities has little or no effect. This finding suggests that VNS may affect memory processes by modulating neural plasticity in brain structures associated with memory storage such as the hippocampus. To test this hypothesis, the present study investigated the modulatory effect of VNS on the development of long-term potentiation (LTP) in the dentate gyrus of freely-moving rats. Rats receiving 0.4 mA VNS showed enhanced potentiation of the population spike amplitude for at least 24 h after tetanus relative to the sham-stimulation group. In contrast, no such effect was observed with 0.2 mA VNS. Stimulation at 0.8 mA had a short-term effect and tended to

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

Fogel SM, Smith CT (2006)MEDLINE-indexed journal, not yet read by usJournal of sleep research237 citations

Learning-dependent changes in sleep spindles and Stage 2 sleep.

It has become increasingly clear that sleep is necessary for efficient memory consolidation. Recently, it has been found that Stage 2 sleep disruption impairs procedural memory performance, and that memory performance is correlated with the duration of Stage 2 sleep; but the mechanisms involved in synaptic plasticity for procedural memory during sleep have not been identified. The present study examined the learning-dependent changes in sleep, including Stage 2 sleep spindles. Following an intense period of simple motor procedural learning, the duration of Stage 2 sleep and spindle density increased. There were no changes observed in the duration of any other stage of sleep or in the density of rapid eye movements. These findings support the hypothesis that sleep spindles are involved in the off-line reprocessing of simple motor procedural memory during Stage 2 sleep.

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

Homozygous and heterozygous disruptions of ANK3: at the crossroads of neurodevelopmental and psychiatric disorders.

AnkyrinG, encoded by the ANK3 gene, is involved in neuronal development and signaling. It has previously been implicated in bipolar disorder and schizophrenia by association studies. Most recently, de novo missense mutations in this gene were identified in autistic patients. However, the causative nature of these mutations remained controversial. Here, we report inactivating mutations in the Ankyrin 3 (ANK3) gene in patients with severe cognitive deficits. In a patient with a borderline intelligence, severe attention deficit hyperactivity disorder (ADHD), autism and sleeping problems, all isoforms of the ANK3 gene, were disrupted by a balanced translocation. Furthermore, in a consanguineous family with moderate intellectual disability (ID), an ADHD-like phenotype and behavioral problems, we identified a homozygous truncating frameshift mutation in the longest isoform of the same gene, wh

matched on Neurogenesis (mesh)

Gay SM, Chartampila E, Lord JS, Grizzard S, Maisashvili T, Ye M, Barker NK, Mordant AL, Mills CA, Herring LE, Diering GH (2024)MEDLINE-indexed journal, not yet read by usProceedings of the National Academy of Sciences of the United States of America14 citations

Developing forebrain synapses are uniquely vulnerable to sleep loss.

Sleep is an essential behavior that supports lifelong brain health and cognition. Neuronal synapses are a major target for restorative sleep function and a locus of dysfunction in response to sleep deprivation (SD). Synapse density is highly dynamic during development, becoming stabilized with maturation to adulthood, suggesting sleep exerts distinct synaptic functions between development and adulthood. Importantly, problems with sleep are common in neurodevelopmental disorders including autism spectrum disorder (ASD). Moreover, early life sleep disruption in animal models causes long-lasting changes in adult behavior. Divergent plasticity engaged during sleep necessarily implies that developing and adult synapses will show differential vulnerability to SD. To investigate distinct sleep functions and mechanisms of vulnerability to SD across development, we systematically examined the beh

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

Closed-loop neuromodulation restores network connectivity and motor control after spinal cord injury.

Recovery from serious neurological injury requires substantial rewiring of neural circuits. Precisely-timed electrical stimulation could be used to restore corrective feedback mechanisms and promote adaptive plasticity after neurological insult, such as spinal cord injury (SCI) or stroke. This study provides the first evidence that closed-loop vagus nerve stimulation (CLV) based on the synaptic eligibility trace leads to dramatic recovery from the most common forms of SCI. The addition of CLV to rehabilitation promoted substantially more recovery of forelimb function compared to rehabilitation alone following chronic unilateral or bilateral cervical SCI in a rat model. Triggering stimulation on the most successful movements is critical to maximize recovery. CLV enhances recovery by strengthening synaptic connectivity from remaining motor networks to the grasping muscles in the forelimb.

matched on Neuronal Plasticity (mesh), Motor Cortex (mesh)

Meyers EC, Solorzano BR, James J, Ganzer PD, Lai ES, Rennaker RL, Kilgard MP, Hays SA (2018)MEDLINE-indexed journal, not yet read by usStroke184 citations

Vagus Nerve Stimulation Enhances Stable Plasticity and Generalization of Stroke Recovery.

Background and purpose: Chronic impairment of the arm and hand is a common consequence of stroke. Animal and human studies indicate that brief bursts of vagus nerve stimulation (VNS) in conjunction with rehabilitative training improve recovery of motor function after stroke. In this study, we tested whether VNS could promote generalization, long-lasting recovery, and structural plasticity in motor networks. Methods: Rats were trained on a fully automated, quantitative task that measures forelimb supination. On task proficiency, unilateral cortical and subcortical ischemic lesions were administered. One week after ischemic lesion, rats were randomly assigned to receive 6 weeks of rehabilitative training on the supination task with or without VNS. Rats then underwent 4 weeks of testing on a task assessing forelimb strength to test generalization of recovery. Finally, the durability of VNS

matched on Neuronal Plasticity (mesh), Motor Cortex (mesh)

Borland MS, Vrana WA, Moreno NA, Fogarty EA, Buell EP, Sharma P, Engineer CT, Kilgard MP (2016)MEDLINE-indexed journal, not yet read by usBrain stimulation99 citations

Cortical Map Plasticity as a Function of Vagus Nerve Stimulation Intensity.

Background: Pairing sensory or motor events with vagus nerve stimulation (VNS) can reorganize sensory or motor cortex. Repeatedly pairing a tone with a brief period of VNS increases the proportion of primary auditory cortex (A1) responding to the frequency of the paired tone. However, the relationship between VNS intensity and cortical map plasticity is not known. Objective/hypothesis: The primary goal of this study was to determine the range of VNS intensities that can be used to direct cortical map plasticity. Methods: The rats were exposed to a 9 kHz tone paired with VNS at intensities of 0.4, 0.8, 1.2, or 1.6 mA. Results: In rats that received moderate (0.4-0.8 mA) intensity VNS, 75% more cortical neurons were tuned to frequencies near the paired tone frequency. A two-fold effective range is broader than expected based on previous VNS studies. Rats that received high (1.2-1.6 mA) int

matched on Neuronal Plasticity (mesh), Motor Cortex (mesh)

Kühn S, Gleich T, Lorenz RC, Lindenberger U, Gallinat J (2014)MEDLINE-indexed journal, not yet read by usMolecular psychiatry193 citations

Playing Super Mario induces structural brain plasticity: gray matter changes resulting from training with a commercial video game.

Video gaming is a highly pervasive activity, providing a multitude of complex cognitive and motor demands. Gaming can be seen as an intense training of several skills. Associated cerebral structural plasticity induced has not been investigated so far. Comparing a control with a video gaming training group that was trained for 2 months for at least 30 min per day with a platformer game, we found significant gray matter (GM) increase in right hippocampal formation (HC), right dorsolateral prefrontal cortex (DLPFC) and bilateral cerebellum in the training group. The HC increase correlated with changes from egocentric to allocentric navigation strategy. GM increases in HC and DLPFC correlated with participants' desire for video gaming, evidence suggesting a predictive role of desire in volume change. Video game training augments GM in brain areas crucial for spatial navigation, strategic pla

matched on Neuronal Plasticity (mesh), Hippocampus (mesh)

Nutritional omega-3 deficiency abolishes endocannabinoid-mediated neuronal functions.

The corollaries of the obesity epidemic that plagues developed societies are malnutrition and resulting biochemical imbalances. Low levels of essential n-3 polyunsaturated fatty acids (n-3 PUFAs) have been linked to neuropsychiatric diseases, but the underlying synaptic alterations are mostly unknown. We found that lifelong n-3 PUFAs dietary insufficiency specifically ablates long-term synaptic depression mediated by endocannabinoids in the prelimbic prefrontal cortex and accumbens. In n-3-deficient mice, presynaptic cannabinoid CB(1) receptors (CB(1)Rs) normally responding to endocannabinoids were uncoupled from their effector G(i/o) proteins. Finally, the dietary-induced reduction of CB(1)R functions in mood-controlling structures was associated with impaired emotional behavior. These findings identify a plausible synaptic substrate for the behavioral alterations caused by the n-3 PUFA

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

Donlea JM, Ramanan N, Shaw PJ (2009)MEDLINE-indexed journal, not yet read by usScience (New York, N.Y.)202 citations

Use-dependent plasticity in clock neurons regulates sleep need in Drosophila.

Sleep is important for memory consolidation and is responsive to waking experience. Clock circuitry is uniquely positioned to coordinate interactions between processes underlying memory and sleep need. Flies increase sleep both after exposure to an enriched social environment and after protocols that induce long-term memory. We found that flies mutant for rutabaga, period, and blistered were deficient for experience-dependent increases in sleep. Rescue of each of these genes within the ventral lateral neurons (LNVs) restores increased sleep after social enrichment. Social experiences that induce increased sleep were associated with an increase in the number of synaptic terminals in the LNV projections into the medulla. The number of synaptic terminals was reduced during sleep and this decline was prevented by sleep deprivation.

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

Dhond RP, Yeh C, Park K, Kettner N, Napadow V (2008)MEDLINE-indexed journal, not yet read by usPain217 citations

Acupuncture modulates resting state connectivity in default and sensorimotor brain networks.

Previous studies have defined low-frequency, spatially consistent networks in resting fMRI data which may reflect functional connectivity. We sought to explore how a complex somatosensory stimulation, acupuncture, influences intrinsic connectivity in two of these networks: the default mode network (DMN) and sensorimotor network (SMN). We analyzed resting fMRI data taken before and after verum and sham acupuncture. Electrocardiography data were used to infer autonomic modulation through measures of heart rate variability (HRV). Probabilistic independent component analysis was used to separate resting fMRI data into DMN and SMN components. Following verum, but not sham, acupuncture there was increased DMN connectivity with pain (anterior cingulate cortex (ACC), periaqueductal gray), affective (amygdala, ACC), and memory (hippocampal formation, middle temporal gyrus) related brain regions.

matched on Neuronal Plasticity (mesh), Motor Cortex (mesh)

Stuber GD, Klanker M, de Ridder B, Bowers MS, Joosten RN, Feenstra MG, Bonci A (2008)MEDLINE-indexed journal, not yet read by usScience (New York, N.Y.)250 citations

Reward-predictive cues enhance excitatory synaptic strength onto midbrain dopamine neurons.

Using sensory information for the prediction of future events is essential for survival. Midbrain dopamine neurons are activated by environmental cues that predict rewards, but the cellular mechanisms that underlie this phenomenon remain elusive. We used in vivo voltammetry and in vitro patch-clamp electrophysiology to show that both dopamine release to reward predictive cues and enhanced synaptic strength onto dopamine neurons develop over the course of cue-reward learning. Increased synaptic strength was not observed after stable behavioral responding. Thus, enhanced synaptic strength onto dopamine neurons may act to facilitate the transformation of neutral environmental stimuli to salient reward-predictive cues.

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

Froemke RC, Merzenich MM, Schreiner CE (2007)MEDLINE-indexed journal, not yet read by usNature482 citations

A synaptic memory trace for cortical receptive field plasticity.

Receptive fields of sensory cortical neurons are plastic, changing in response to alterations of neural activity or sensory experience. In this way, cortical representations of the sensory environment can incorporate new information about the world, depending on the relevance or value of particular stimuli. Neuromodulation is required for cortical plasticity, but it is uncertain how subcortical neuromodulatory systems, such as the cholinergic nucleus basalis, interact with and refine cortical circuits. Here we determine the dynamics of synaptic receptive field plasticity in the adult primary auditory cortex (also known as AI) using in vivo whole-cell recording. Pairing sensory stimulation with nucleus basalis activation shifted the preferred stimuli of cortical neurons by inducing a rapid reduction of synaptic inhibition within seconds, which was followed by a large increase in excitatio

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

Hu H, Real E, Takamiya K, Kang MG, Ledoux J, Huganir RL, Malinow R (2007)MEDLINE-indexed journal, not yet read by usCell370 citations

Emotion enhances learning via norepinephrine regulation of AMPA-receptor trafficking.

Emotion enhances our ability to form vivid memories of even trivial events. Norepinephrine (NE), a neuromodulator released during emotional arousal, plays a central role in the emotional regulation of memory. However, the underlying molecular mechanism remains elusive. Toward this aim, we have examined the role of NE in contextual memory formation and in the synaptic delivery of GluR1-containing alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA)-type glutamate receptors during long-term potentiation (LTP), a candidate synaptic mechanism for learning. We found that NE, as well as emotional stress, induces phosphorylation of GluR1 at sites critical for its synaptic delivery. Phosphorylation at these sites is necessary and sufficient to lower the threshold for GluR1 synaptic incorporation during LTP. In behavioral experiments, NE can lower the threshold for memory formation in

matched on Long-Term Potentiation (mesh), Hippocampus (mesh), Synapses (mesh)

Yu H, Wang DD, Wang Y, Liu T, Lee FS, Chen ZY (2012)MEDLINE-indexed journal, not yet read by usThe Journal of neuroscience : the official journal of the Society for Neuroscience220 citations

Variant brain-derived neurotrophic factor Val66Met polymorphism alters vulnerability to stress and response to antidepressants.

Brain-derived neurotrophic factor (BDNF) plays important roles in cell survival, neural plasticity, learning, and stress regulation. However, whether the recently found human BDNF Val66Met (BDNF(Met)) polymorphism could alter stress vulnerability remains controversial. More importantly, the molecular and structural mechanisms underlying the interaction between the BDNF(Met) polymorphism and stress are unclear. We found that heterozygous BDNF(+/Met) mice displayed hypothalamic-pituitary-adrenal axis hyperreactivity, increased depressive-like and anxiety-like behaviors, and impaired working memory compared with WT mice after 7 d restraint stress. Moreover, BDNF(+/Met) mice exhibited more prominent changes in BDNF levels and apical dendritic spine density in the prefrontal cortex and amygdala after stress, which correlated with the impaired working memory and elevated anxiety-like behaviors

matched on Brain-Derived Neurotrophic Factor (mesh), Dendritic Spines (mesh)

Coluk Y, Yildirim G, Yildirmak S, Peker EGG (2025)MEDLINE-indexed journal, not yet read by usBMC neurology3 citations

Altered brain-derived neurotrophic factor levels and oxidative stress in REM sleep deprivation: a rat model study.

Background: Brain-derived neurotrophic factor (BDNF) is among the modulators associated with cognition and sleep that play a role in sleep disorders. This study aimed at investigating the effects of chronic sleep deprivation and REM sleep deprivation on BDNF levels and oxidative stress markers. Methods: A total of 24 healthy male Wistar albino rats were separated into 3 groups as REM sleep deprivation group, control sleep deprivation group and control group. To create models of 21-day REM sleep deprivation and control sleep deprivation, we used the platform technique. After 21 days blood BDNF, brain tissue BDNF, brain tissue malondialdehyde, glutathione, ascorbic acid, nitrite and nitrate were evaluated. Results: Compared with the control group, control sleep deprivation group showed a significant increase in brain tissue levels of BDNF (p = 0.038), whereas a significant decrease was obs

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

Ning Y, Feng S, Zheng S, Wu Z, Liu X, Dong L, Jia H (2024)MEDLINE-indexed journal, not yet read by usSleep medicine4 citations

How BDNF affects working memory in acute sleep deprivation: The mediating role of spontaneous brain activity.

The brain-derived neurotrophic factor (BDNF) mediates the plasticity associated with memory processing, and compensatorily increases after acute sleep deprivation (SD). However, whether the altered spontaneous brain activity mediates the association between BDNF and working memory in SD remains unknown. Here, we aimed to probe the mediating role of the spontaneous brain activity between plasma BDNF and WM function in SD. A total of 30 healthy subjects with regular sleep were enrolled in this study. Resting-sate functional magnetic resonance imaging (fMRI) scans and the peripheral blood were collected before and after 24 h SD. All participants also received n-back task assessing working memory (WM) performance. The amplitude of low-frequency fluctuation (ALFF) and fractional ALFF (fALFF) were calculated to reflect the intensity of regional spontaneous brain activity. Plasma BDNF was measu

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

Håkansson K, Ledreux A, Daffner K, Terjestam Y, Bergman P, Carlsson R, Kivipelto M, Winblad B, Granholm AC, Mohammed AK (2017)MEDLINE-indexed journal, not yet read by usJournal of Alzheimer's disease : JAD139 citations

BDNF Responses in Healthy Older Persons to 35 Minutes of Physical Exercise, Cognitive Training, and Mindfulness: Associations with Working Memory Function.

Brain-derived neurotrophic factor (BDNF) has a central role in brain plasticity by mediating changes in cortical thickness and synaptic density in response to physical activity and environmental enrichment. Previous studies suggest that physical exercise can augment BDNF levels, both in serum and the brain, but no other study has examined how different types of activities compare with physical exercise in their ability to affect BDNF levels. By using a balanced cross over experimental design, we exposed nineteen healthy older adults to 35-minute sessions of physical exercise, cognitive training, and mindfulness practice, and compared the resulting changes in mature BDNF levels between the three activities. We show that a single bout of physical exercise has significantly larger impact on serum BDNF levels than either cognitive training or mindfulness practice in the same persons. This is

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

Bowles S, Hickman J, Peng X, Williamson WR, Huang R, Washington K, Donegan D, Welle CG (2022)MEDLINE-indexed journal, not yet read by usNeuron102 citations

Vagus nerve stimulation drives selective circuit modulation through cholinergic reinforcement.

Vagus nerve stimulation (VNS) is a neuromodulation therapy for a broad and expanding set of neurologic conditions. However, the mechanism through which VNS influences central nervous system circuitry is not well described, limiting therapeutic optimization. VNS leads to widespread brain activation, but the effects on behavior are remarkably specific, indicating plasticity unique to behaviorally engaged neural circuits. To understand how VNS can lead to specific circuit modulation, we leveraged genetic tools including optogenetics and in vivo calcium imaging in mice learning a skilled reach task. We find that VNS enhances skilled motor learning in healthy animals via a cholinergic reinforcement mechanism, producing a rapid consolidation of an expert reach trajectory. In primary motor cortex (M1), VNS drives precise temporal modulation of neurons that respond to behavioral outcome. This su

matched on Neuronal Plasticity (mesh), Motor Cortex (keyword)

Allsopp RC, Hernández LM, Taylor MK (2024)MEDLINE-indexed journal, not yet read by usScientific reports1 citations

The Val66Met variant of brain-derived neurotrophic factor is linked to reduced telomere length in a military population: a pilot study.

In military populations, gene-environment interactions can influence performance and health outcomes. Brain-derived neurotrophic factor (BDNF) is a central nervous system protein that is important for neuronal function and synaptic plasticity. A BDNF single nucleotide polymorphism, rs6265, leads to an amino acid substitution of valine (Val) with methionine (Met) at codon 66 (Val66Met), which may influence an individual's response to occupational stress, and predispose military members to psychological disorders. Telomere length (TL), a novel measure of biological aging, can be used as a biomarker of stress. Accordingly, telomere shortening may be a surrogate indicator of physiological weathering due to chronic disease and stressful life events. To increase our understanding about the potential effect of the Val66Met mutation on the human stress response, we evaluated the relationships be

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

Nigam SM, Xu S, Kritikou JS, Marosi K, Brodin L, Mattson MP (2017)MEDLINE-indexed journal, not yet read by usJournal of neurochemistry157 citations

Exercise and BDNF reduce Aβ production by enhancing α-secretase processing of APP.

Alzheimer's disease (AD) is an age-related neurodegenerative disorder characterized by aggregation of toxic forms of amyloid β peptide (Aβ). Treatment strategies have largely been focused on inhibiting the enzymes (β- and γ-secretases) that liberate Aβ from the amyloid precursor protein (APP). While evidence suggests that individuals who exercise regularly are at reduced risk for AD and studies of animal models demonstrate that running can ameliorate brain Aβ pathology and associated cognitive deficits, the underlying mechanisms are unknown. However, considerable evidence suggests that brain-derived neurotrophic factor (BDNF) mediates beneficial effects of exercise on neuroplasticity and cellular stress resistance. Here, we tested the hypothesis that BDNF promotes non-amyloidogenic APP processing. Using a transgenic mouse model of Alzheimer's disease and cultured human neural cells, we d

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

Adzic M, Djordjevic J, Mitic M, Brkic Z, Lukic I, Radojcic M (2015)MEDLINE-indexed journal, not yet read by usBehavioural brain research60 citations

The contribution of hypothalamic neuroendocrine, neuroplastic and neuroinflammatory processes to lipopolysaccharide-induced depressive-like behaviour in female and male rats: Involvement of glucocorticoid receptor and C/EBP-β.

Peripheral inflammation induced by lipopolysaccharide (LPS) causes behavioural changes indicative for depression. The possible mechanisms involve the interference with neuroinflammatory, neuroendocrine, and neurotrophic processes. Apart from heterogeneity in the molecular background, sexual context may be another factor relevant to the manifestation of mood disturbances upon an immune challenge. We investigated sex-dependent effects of a 7-day LPS treatment of adult Wistar rats on depressive-like behaviour and their relation with hypothalamic neuroendocrine factor, corticotrophin-releasing hormone (CRH), proplastic brain-derived neurotropic factor (BDNF), pro-inflammatory cyclooxygenase-2 (COX-2) and nuclear factor kappa beta (NFkB). Also, their regulators, the glucocorticoid receptor (GR) and CCAAT enhancer-binding protein (C/EBP) β were followed. LPS induced depressive-like behaviour i

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