Plasticity in the Adult Brain: From Genes to Neurotherapy (Progress in Brain Research)
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While the practice grew slowly in the decades after Sterman's initial work, recent advances in technology and processor speeds have allowed more practitioners to offer the services with less of an investment, and a consensus has arisen based on research that peaked in the early aughts that the brain is in fact neuroplastic. Neurofeedback has shown demonstrable results in hundreds of patients over the past few decades, Little says, with more than peer-reviewed research articles published on the topic in the past few years alone. Robert Longo, a Lexington, North Carolina, counselor on the board of directors for the International Society for Neurofeedback and Research, says it's now widely accepted that the notion of rewiring the brain isn't hocus-pocus.
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It's very clear now that it works," says Little. I first stumbled across the concept of neurofeedback while researching a story on anger in A couple of the experts I interviewed mentioned the practice, and I found a company called Brain State Technologies that offered a neurofeedback treatment it called Brainwave Optimization.
The company connected me with a practitioner in New York City, and in April that year I underwent two sessions. After the first session, I felt as if I'd just finished meditating, and the world seemed a little brighter. After the second, I felt like I'd taken a Xanax. More committed users sometimes—though not always—see even more dramatic and long-lasting effects.
Longo's wife, for example, started using neurofeedback after she fell down a flight of stairs and suffered a series of headaches and vertigo.
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After 30 sessions, "it made a percent difference," she says. But there's a growing amount of literature and research, and in the next five or 10 years you're going to see a lot of support when we say we can treat things like traumatic brain injuries, anxiety, depression, ADHD, insomnia, migraine headaches and people who have had strokes.
Charles Tegeler, a neurology professor at Wake Forest Baptist Medical Center in North Carolina, got into the field after running a stroke center for 15 years. He became increasingly concerned that stress was killing people, he says, and "putting people on drugs was just a big Band-Aid. But his daughter had developed migraine headaches so excruciating she'd missed most of her classes during the previous semester.
Tegeler decided she could undergo the company's brain wave optimization. Tegeler also tried it himself, to see if it could do anything for his irregular heartbeat. After 10 sessions in five days, Tegeler's heart was back to normal, and his daughter's headaches were gone. In , he founded a research institute at Wake Forest called HIRREM, which stands for "high-resolution, relational, resonance-based, electroencephalic mirroring. Essentially, the fiber optic cables are designed to light up under electrical stimulation, and a protein would be added to a neuron via gene therapy to excite it under light stimuli.
Neuromodulation offers a wide degree of therapy for many patients, but due to the nature of the disorders it is currently used to treat its effects are often temporary. Future goals in the field hope to alleviate that problem by increasing the years of effect until DBS can be used for the remainder of the patient's life. Another use for neuromodulation would be in building neuro-interface prosthetic devices that would allow quadriplegics the ability to maneuver a cursor on a screen with their thoughts, thereby increasing their ability to interact with others around them.
By understanding the motor cortex and understanding how the brain signals motion, it is possible to emulate this response on a computer screen. The ethical debate about use of embryonic stem cells has stirred controversy both in the United States and abroad; although more recently these debates have lessened due to modern advances in creating induced pluripotent stem cells from adult cells. The greatest advantage for use of embryonic stem cells is the fact that they can differentiate become nearly any type of cell provided the right conditions and signals.
However, recent advances by Shinya Yamanaka et al. However, induced pluripotent cells have the potential to form benign though potentially malignant tumors, and tend to have poor survivability in vivo in the living body on damaged tissue. Enhancements of traits, use of animals for tissue scaffolding, and even arguments for moral degeneration have been made with the fears that if this technology reaches its full potential a new paradigm shift will occur in human behavior.
New neurotechnologies have always garnered the appeal of governments, from lie detection technology and virtual reality to rehabilitation and understanding the psyche. By combining pharmaceuticals and neurotechnologies, some researchers have discovered ways of lowering the "fear" response and theorize that it may be applicable to PTSD. If improved, it could be possible to train soldiers how to deal with complex situations in times of peace, in order to better prepare and train a modern army.
UZH - Neuroscience Center Zurich - Cognitive Neuroscience
Finally, when these technologies are being developed society must understand that these neurotechnologies could reveal the one thing that people can always keep secret: what they are thinking. While there are large amounts of benefits associated with these technologies, it is necessary for scientists, citizens and policy makers alike to consider implications for privacy.
Cognitive liberty refers to a suggested right to self-determination of individuals to control their own mental processes, cognition, and consciousness including by the use of various neurotechnologies and psychoactive substances. This perceived right is relevant for reformation and development of associated laws. From Wikipedia, the free encyclopedia. This section is written like a personal reflection, personal essay, or argumentative essay that states a Wikipedia editor's personal feelings or presents an original argument about a topic.
Please help improve it by rewriting it in an encyclopedic style. June Learn how and when to remove this template message. Frontiers in Human Neuroscience. BrainAge Based on the work of Ryuta Kawashima , M.
Broman; Jack Fletcher The changing nervous system: neurobehavioral consequences of early brain disorders. Oxford University Press US. Viking Adult. Physiology of Behavior. Neuroscience, Fourth Edition. Sinauer Associates, Inc. Proceedings of the National Academy of Sciences. Bibcode : PNAS.. Behavioural Neurology. Nanomedicine: Nanotechnology, Biology and Medicine. Nature Communications. Bibcode : NatCo The European Journal of Neuroscience. Lay summary.
Cathodal tDCS compared with sham decreased learning rates during training and resulted in poorer performance which lasted over 24 h after stimulation. Anodal tDCS showed an operation-specific improvement for subtraction learning. We found that stimulation of dlPFC significantly increased recollection accuracy, relative to a no-stimulation sham condition and also relative to active stimulation of a comparison region in left parietal cortex.
November Athinoula A. Martinos Center for Biomedical Imaging.
Electroencephalography and Clinical Neurophysiology. Clinical Neurophysiology. Magnetic Resonance in Medicine. Journal of Forensic Sciences. Bibcode : Sci Nature Medicine. Cell Stem Cell. Retrieved November 24, Toxicological Sciences. Journal of Neurochemistry. Unfortunately, relatively high doses of BDNF need to be administered to achieve these behavioral responses. Several studies have suggested that normal BDNF signaling is both necessary and sufficient for antidepressant drug action. Chronic, but not acute, administration of several different types of antidepressants, including SSRIs, a NE-selective reuptake inhibitor, a monoamine oxidase inhibitor, an atypical antidepressant, ECS, and lithium, increase the levels of CREB mRNA and immunoreactivity in hippocampus In situ hybridization and immunohistochemical analysis demonstrate that the expression of CREB is increased in the major cell layers of hippocampus ie , CA3 and CA1 pyramidal and dentate gyrus granule cell layers.
In contrast, chronic administration of nonantidepressant psychotropic drugs ie , morphine, cocaine, and haloperidol does not influence the expression of CREB in hippocampus, demonstrating the pharmacologic specificity of this effect for antidepressants. In fact, chronic opiate or psychostimulant treatments are reported to regulate CREB in striatum and locus coeruleus This demonstrates that CREB is regulated in a region-specific manner depending on the neurotransmitter systems influenced by these psychotropic drug treatments. Hippocampal overexpression of BDNF or CREB is capable of mimicking both the structural consequences of sustained antidepressant treatment as well as exerting antidepressant-like behavioral effects 61 , Indeed, activation of the cAMP-CREB cascade results in increased neurogenesis of dentate granule cell progenitors, and increased dendritic length and branching BDNF, in addition to being a target of CREB, can itself recruit this particular transcription factor by activating the mitogen-activated protein MAP kinase cascade 66 , thus setting up a potential positive feed-back loop.
Taken together, elevated BDNF-CREB, through their protective influences on vulnerable hippocampal neurons and their ability to directly promote structural reorganization, could result in repair of this region known to be damaged in depression. In addition, BDNF can alter neurotransmitter release and itself elicit an activation of postsynaptic neurons, and may thus have potential protective functional consequences on hippocampal circuitry known to be dysfunctional in depression A direct consequence of enhanced hippocampal function would be a restoration of the inhibitory control exerted on the stress response pathway of the HPA axis.
In addition, the well-established role of BDNF and CREB in hippocampal-dependent learning and memory may play a critical role in ameliorating the cognitive symptoms associated with depression 67 , Therefore, reduced BDNF levels result in neuronal atrophy and cell death in the hippocampus whereas enhanced BDNF levels are associated with neurogenesis, cell survival and dendritic arborization.
The role of BDNF in depression on the basis of its location in the neural circuitry
Thus, changes in hippocampal BDNF levels and the resulting downstream signaling pathways may play an essential role in regulating depression related behaviors. Several lines of evidence suggest that the prefrontal cortex PFC is involved in the neuropathology of depression and the response to stress. Perhaps the most widely accepted division of PFC, based on anatomical connectivity and functional specialization, is the dorsolateral and ventromedial sectors The ventromedial prefrontal cortex vmPFC includes the ventral portion of the medial prefrontal cortex and medial portion of the orbital surface.
Targets of vmPFC projections include the hypothalamus and periaqueductal gray, which mediate the visceral autonomic activity associated with emotion, and the ventral striatum, which signals reward and motivational value. In addition, vmPFC has dense reciprocal connections with the amygdala, which is involved in threat detection and fear conditioning By contrast, the dorsolateral prefrontal cortex DLPFC , which includes portions of the middle and superior frontal gyri on the lateral surface of the frontal lobes, receives input from specific sensory cortices, and has dense interconnections with premotor areas, the frontal eye fields, and lateral parietal cortex The distinct patterns of connectivity in these two regions of PFC suggest disparate functionality.
Volumetric changes in the PFC in depression are similar to those described in the human hippocampus. The earliest functional imaging studies of depression compared the resting state brain activity eg blood flow or glucose metabolism of depressed patients with that of non-depressed comparison subjects.
Results from these studies associate depression with abnormally high levels of vmPFC activity 71 , but abnormally low levels of DLPFC activity in resting brain activity Recent, a type of functional imaging study compares task-related brain activations blood flow of depressed patients to that of non-depressed comparison subjects.
Data from these studies demonstrate that depressed patients exhibit greater task-related activation in DLPFC during tests of working memory and cognitive control when performance is matched to non-depressed subjects However, functional imaging data alone cannot adjudicate whether the abnormal activity profiles observed in vmPFC and DLPFC are a cause or consequence of the disorder.
In humans, postmortem studies have shown that both BDNF and TrkB levels are significantly decreased in the prefrontal cortex and hippocampus of suicide patients compared with controls and antidepressant therapy restores brain BDNF levels to the normal range In addition, there were significant decreases in the phosphorylation of TrkA and TrkB in both PFC and hippocampus of suicide subjects, whereas the phosphorylation of TrkC was decreased only in hippocampus without any change in PFC Stress is used as a model to study alterations of molecules and brain structure because mood disorders are often precipitated or exacerbated by acute or chronic stressful life events Repeated stress causes dendritic shortening in medial prefrontal cortex, as well as in hippocampus The failure of desipramine to positively modulate BDNF and TrkB expression in postnatal day 13 rats is consistent with the lack of efficacy of desipramine in children and adolescents In hippocampus, chronic fluoxetine administration led to a 2.
These studies demonstrate that chronic administration of fluoxetine leads to brain region specific upregulation of BDNF in the adult brain, which suggests that chronically administered antidepressants could promote BDNF-induced gene expression and synaptic plasticity in multiple brain regions. Animals work shows that stress decreases phosphorylated CREB and antidepressants treatment increases the expression of phosphorylated CREB specifically in the hippocampus and prefrontal cortex Experimental studies demonstrated that chronic forced swim stress decreased the expression of phosphorylated-extracellular signal-regulated kinase 2 p-ERK2 , ERK1 and ERK2 in the hippocampus and prefrontal cortex in rats; fluoxetine reversed the stress-induced disruption of the p-ERK2, which is indicated by the increased level of the p-ERK2 in the hippocampus and prefrontal cortex in stress-fluoxetine group compared to stress group, but exhibited no effect on the stress-induced decrease of the ERK1 and ERK2.
The NAc is a target of the mesolimbic dopamine system, which receives dopamine input from dopaminergic neurons in the ventral tegmental area VTA of the midbrain. Furthermore, the ventral striatum also has been noted to have extensive connections with the amygdala and the orbital, subgenual, and ventrolateral PFC The NAc, and its dopaminergic inputs, play critical roles in reward. Virtually all drugs of abuse increase dopaminergic transmission in the NAc, which partly mediates their rewarding effects On the other hand, the VTA neurons also innervate several other limbic structures, including the amygdala and limbic regions of neocortex.
The relationship of VTA-NAc pathway to mood disorders requires further study, but it seems plausible that disturbances in this pathway would be related to abnormalities in hedonic tone and motivation 2 , which are central features of mania and depression. This is supported by the finding of decreased striatal response to happy stimuli associated with level of anhedonia in depressed subjects as well as the observation of increased striatal activity in mania At the same time, intra-VTA infusion of BDNF exerts a depression-like effect in the forced swim test, while blockade of BDNF action in the NAc, by use of viral-mediated overexpression of a dominant negative mutant of TrkB, causes an antidepressant-like effect in the same test While dysfunction of the VTA-NAc circuit is thought to be associated with depression, antidepressants have been postulated to reverse this dysfunction.
CREB is known to positively modulate levels of dynorphin within the NAc 88 , and this upregulation of the endogenous opioid dynorphin could mediate the pro-depressive effects of CREB. Although at present it is unknown if CREB induction in the NAc results in enhanced dynorphin release within the VTA, it has been hypothesized that such a change in the context of the VTA-NAc pathway could result in dysphoria and lack of pleasure seeking This raises the possibility that enhanced BDNF-CREB in the NAc may, through a regulation of opioid signalling, result in an anhedonic state thus contributing to the pro-depressive effects, whereas an abrogation of BDNF-CREB signalling in this region could have beneficial consequences on behavior and exert an antidepressant-like effect.
The opposite behavioral response for infusion BDNF to hippocampus versus NAc suggests that depression and antidepressant effects are related to the functional consequences of different downstream regulation in different neuronal networks.