Posts Tagged Alzheimer’s disease

[WEB SITE] Nootropics: Types, safety, and risks of smart drugs

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Nootropics, or “smart drugs,” are a class of substances that can boost brain performance. They are sometimes called cognition enhancers or memory enhancing substances.

Prescription nootropics are medications that have stimulant effects. They can counteract the symptoms of medical conditions such as attention deficit hyperactivity disorder (ADHD), narcolepsy, or Alzheimer’s disease.

Nonprescription substances that can enhance brain performance or focus — such as caffeine and creatine — are also considered nootropics. They do not treat diseases but may have some effects on thinking, memory, or other mental functions.

This article looks at prescription and nonprescription smart drugs, including their uses, side effects, and safety warnings.

Prescription nootropics

a woman taking nootropics at her desk.

A person may take a nootropic to treat ADHD, narcolepsy, or dementia.

Prescription nootropics include:

  • modafinil (Provigil), a stimulant that addresses the sudden drowsiness of narcolepsy
  • Adderall, which contains amphetamines to treat ADHD
  • methylphenidate (Ritalin), a stimulant that can manage symptoms of narcolepsy and ADHD
  • memantine (Axura), which treats symptoms of Alzheimer’s disease

While these can be effective in treating specific medical conditions, a person should not take them without a prescription.

Like any prescription medications, they carry risks of side effects and interactions, and a person should only take them under a doctor’s care.

Common side effects of prescription nootropics include:

Some evidence suggests that people who use prescription nootropics to improve brain function have a higher risk of impulsive behaviors, such as risky sexual practices.

Healthcare providers should work closely with people taking prescription nootropics to manage any side effects and monitor their condition.

Over-the-counter nootropics

The term “nootropic” can also refer to natural or synthetic supplements that boost mental performance. The following sections discuss nootropics that do not require a prescription.

Caffeine

Many people consume beverages that contain caffeine, such as coffee or tea, because of their stimulant effects. Studies suggest that caffeine is safe for most people in moderate amounts.

Having a regular cup of coffee or tea may be a good way to boost mental focus. However, extreme amounts of caffeine may not be safe.

The Food and Drug Administration (FDA) recommend that people consume no more than 400 milligrams (mg) of caffeine a day. This is the amount in 4–5 cups of coffee.

Caffeine pills and powders can contain extremely high amounts of the stimulant. Taking them can lead to a caffeine overdose and even death, in rare cases.

Women who are pregnant or may become pregnant may need to limit or avoid caffeine intake. Studies have found that consuming 4 or more servings of caffeine a day is linked to a higher risk of pregnancy loss.

L-theanine

L-theanine is an amino acid that occurs in black and green teas. People can also take l-theanine supplements.

A 2016 review reported that l-theanine may increase alpha waves in the brain. Alpha waves may contribute to a relaxed yet alert mental state.

L-theanine may work well when paired with caffeine. Some evidence suggests that this combination helps boost cognitive performance and alertness. Anyone looking to consume l-theanine in tea should keep the FDA’s caffeine guidelines in mind.

There are no dosage guidelines for l-theanine, but many supplements recommend taking 100–400 mg per day.

Omega-3 fatty acids

person at desk holding omega 3 supplements in palm

Studies have shown that omega-3 fatty acids are important to fight against brain aging.

These polyunsaturated fats are found in fatty fish and fish oil supplements. This type of fat is important for brain health, and a person must get it from their diet.

Omega-3s help build membranes around the body’s cells, including the neurons. These fats are important for repairing and renewing brain cells.

A 2015 review found that omega-3 fatty acids protect against brain aging. Other research has concluded that omega-3s are important for brain and nervous system function.

However, a large analysis found “no benefit for cognitive function with omega‐3 [polyunsaturated fatty acids] supplementation among cognitively healthy older people.” The authors recommend further long term studies.

A person can get omega-3 supplements in various forms, including fish oil, krill oil, and algal oil.

These supplements carry a low risk of side effects when a person takes them as directed, but they may interact with medications that affect blood clotting. Ask a doctor before taking them.

Racetams

Racetams are synthetic compounds that can affect neurotransmitters in the brain. Some nootropic racetams include:

  • piracetam
  • pramiracetam
  • phenylpiracetam
  • aniracetam

A study conducted in rats suggests that piracetam may have neuroprotective effects.

One review states that “Some of the studies suggested there may be some benefit from piracetam, but, overall, the evidence is not consistent or positive enough to support its use for dementia or cognitive impairment.” Confirming this will require more research.

There is no set dosage for racetams, so a person should follow instructions and consult a healthcare provider. Overall, studies have no found adverse effects of taking racetams as directed.

Ginkgo biloba

Ginkgo biloba is a tree native to China, Japan, and Korea. Its leaves are available as an herbal supplement.

2016 study found that gingko biloba is “potentially beneficial” for improving brain function, but confirming this will require more research.

Ginkgo biloba may help with dementia symptoms, according to one review, which reported the effects occurring in people who took more than 200 mg per day for at least 5 months.

However, the review’s authors note that more research is needed. Also, with prescription nootropics available, ginkgo biloba may not be the most safe or effective option.

Panax ginseng

Panax ginseng is a perennial shrub that grows in China and parts of Siberia. People use its roots for medicinal purposes.

People should not confuse Panax ginseng with other types of ginseng, such as Siberian or American varieties. These are different plants with different uses.

2018 review reports that Panax ginseng may help prevent certain brain diseases, including Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease. It also may help with brain recovery after a stroke.

Panax ginseng interacts with many medications, so consult a doctor before taking it. A typical dosage for mental function is 100–600 mg once or twice a day.

Rhodiola

Some evidence suggests that Rhodiola rosea L., also known as rhodiola or roseroot, can help with cognitive ability.

One review reported that rhodiola may have neuroprotective effects and may help treat neurodegenerative diseases.

Another review found that rhodiola helped regulate neurotransmitters in the brain, having a positive effect on mood.

Rhodiola capsules have varying strengths. Usually, a person takes a capsule once or twice daily.

Creatine

Creatine is an amino acid, which is a building block of protein. This supplement is popular among athletes because it may help improve exercise performance. It may also have some effects on mental ability.

A 2018 review found that taking creatine appears to help with short term memory and reasoning. Whether it helps the brain in other ways is unclear.

The International Society of Sports Nutrition report that creatine supplementation of up to 30 grams per day is safe for healthy people to take for 5 years.

Another 2018 review notes that there has been limited research into whether this supplement is safe and effective for adolescent athletes.

Do nootropics work?

Some small studies show that some nootropic supplements can affect the brain. But there is a lack of evidence from large, controlled studies to show that some of these supplements consistently work and are completely safe.

Because of the lack of research, experts cannot say with certainty that over-the-counter nootropics improve thinking or brain function — or that everyone can safely use them.

For example, one report on cognitive enhancers found that there is not enough evidence to indicate that they are safe and effective for healthy people. The researchers also point to ethical concerns.

However, there is evidence that omega-3 fatty acids can benefit the brain and overall health. In addition, caffeine can improve mental focus in the short term.

Notes on the safety of nootropics

doctor and patient in office discussing adrenal cancer

A person should talk to a doctor about any interactions supplements may have with existing medications.

Also, some supplements may not contain what their labels say. A study of rhodiola products, for example, found that some contain contaminants or other ingredients not listed on the label.

For this reason, it is important to only purchase supplements from reputable companies that undergo independent testing.

BUYING NOOTROPICSA prescription is necessary for some nootropics, such as Provigil and Adderall. Over-the-counter nootropics are available in some supermarkets and drug stores, or people can choose between brands online:

Not all of these supplements are recommended by healthcare providers and some may interact with medications. Always speak to a doctor before trying a supplement.

Summary

Many doctors agree that the best way to boost brain function is to get adequate sleep, exercise regularly, eat a healthy diet, and manage stress.

For people who want to boost their cognitive function, nootropic supplements may help, in some cases. Anyone interested in trying a nootropic should consult a healthcare professional about the best options.

 

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[WEB SITE] Neuroscientists unravel how two different types of brain plasticity work on synapses

 

The brain’s crucial function is to allow organisms to learn and adapt to their surroundings. It does this by literally changing the connections, or synapses, between neurons, strengthening meaningful patterns of neural activity in order to store information. The existence of this process – brain plasticity – has been known for some time.

But actually, there are two different types of brain plasticity at work on synapses. One is “Hebbian plasticity”; it is the one which effectively allows for the recording of information in the synapses, named after pioneering neuroscientist Donald Hebb. The other, more recently discovered, is “homeostatic synaptic plasticity” (HSP), and, like other “homeostatic” processes in the body such as maintaining a constant body temperature, its purpose is to keep things stable. In this case, HSP ensures that the brain doesn’t build up too much activity (as is the case in epilepsy) or become too quiet (as can happen when you lose synapses in Alzheimer’s Disease).

However, little is known about how these two types of plasticity actually interact in the brain. Now, a team of neuroscientists at the Champalimaud Centre for the Unknown, in Lisbon, Portugal, has begun to unravel the fundamental processes that happen in the synapse when the two mechanisms overlap. Their results were published in the journal iScience.

“In theory, the two types of plasticity act as opposing forces”, says Anna Hobbiss, first author of the new study, which was led by Inbal Israely. “Hebbian plasticity reacts to activity at the synapses by inciting them to get stronger while HSP reacts to it by making them weaker. We wanted to understand, on a cellular and molecular level, how the synapse deals with these two forces when they are present at the same time.”

In so doing, the authors have surprisingly shown that, contrary to what might be expected, HSP facilitates Hebbian plasticity, and thus influences memory formation and learning. This means that these two types of plasticity “may actually not be such distinct processes, but instead work together at the same synapses”, says Israely.

The team’s goal was to determine the changes in size of minute structures called dendritic spines, which are the “receiving end” of the synapse. The size of these spines changes to reflect the strength of the synaptic connection.

For this, they studied cells from the mouse hippocampus, a part of the brain which is crucial for learning. In their experiments, they blocked activity in the cells by introducing a potent neurotoxin called tetrodotoxin, thus simulating the loss of input to a certain part of the brain (“think about a person suddenly becoming blind, which leads to loss of input from the eyes to the brain”, says Hobbiss).

Forty eight hours later, they mimicked a small recovery of activity at only one synapse by releasing a few molecules of a neurotransmitter called glutamate on single spines of single neurons. This was possible thanks to a very high resolution, state-of-the-art laser technology, called two-photon microscopy, which allowed the scientists to very precisely visualize and target individual dendritic spines.

As this process evolved, the team closely watched what was happening to the spines – and they saw various anatomical changes. First, the silencing of all neural activity made the spines grow in size. “The spines are like little microphones, which, when there is silence, ramp up the ‘volume’ to try and catch even the faintest noise”, Hobbiss explains.

The scientists then activated individual spines with pulses of glutamate and watched them for two hours. One of the things they thought could happen was that the size of the spines would not grow further, since they had already turned up their ‘volume’ as far is it would go. But the opposite happened: the spines grew even more, with the smaller spines showing the biggest growth.

Finally, the authors also saw growth in neighboring spines, even though the experiment only targeted one spine. “We found that after a lack of activity, other spines in the vicinity also grew, further enhancing the cell’s sensitivity to restored neural transmission”, says Hobbiss. “The cells become more sensitive, more susceptible to encode information. It is as though the ‘gain’ has been turned up”, she adds.

“The fact that neighboring spines grew together with an active spine signifies that homeostatic plasticity changes one of the hallmark features of information storage, which is that plasticity is limited to the site of information entry”, Israely explains. “So, in this sense, the different plasticity mechanisms which are at work in the neuron can cooperate to change which and how many inputs respond to a stimulus. I think this is an exciting finding of our study.”

Taken together, these results show that homeostatic plasticity can actually rev up Hebbian plasticity, the type required for storing information. “Our work adds a piece to the puzzle of how the brain performs one of its fundamental tasks: being able to encode information while still keeping a stable level of activity”, concludes Hobbiss.

The misregulation of homeostatic plasticity – the stabilizing one – has started to be implicated in human health, specifically neurodevelopmental disorders such as Fragile X syndrome and Rett syndrome as well as neurodegenerative ones such as Alzheimer’s Disease. “Perhaps this balance is what allows us to be able to learn new information while retaining stability of that knowledge over a lifetime”, says Israely.

 

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[WEB SITE] Antiepileptic drug use linked to increased risk of Alzheimer’s and dementia

The use of antiepileptic drugs is associated with an increased risk of Alzheimer’s disease and dementia, according to a new study from the University of Eastern Finland and the German Center for Neurodegenerative Diseases, DZNE. Continuous use of antiepileptic drugs for a period exceeding one year was associated with a 15 percent increased risk of Alzheimer’s disease in the Finnish dataset, and with a 30 percent increased risk of dementia in the German dataset.

Some antiepileptic drugs are known to impair cognitive function, which refers to all different aspects of information processing. When the researchers compared different antiepileptic drugs, they found that the risk of Alzheimer’s disease and dementia was specifically associated with drugs that impair cognitive function. These drugs were associated with a 20 percent increased risk of Alzheimer’s disease and with a 60 percent increased risk of dementia.

The researchers also found that the higher the dose of a drug that impairs cognitive function, the higher the risk of dementia. However, other antiepileptic drugs, i.e. those which do not impair cognitive processing, were not associated with the risk.

“More research should be conducted into the long-term cognitive effects of these drugs, especially among older people,” Senior Researcher Heidi Taipale from the University of Eastern Finland says.

Besides for epilepsy, antiepileptic drugs are used in the treatment of neuropathic pain, bipolar disorder and generalized anxiety disorder. This new study is the largest research on the topic so far, and the first to investigate the association in terms of regularity of use, dose and comparing the risk between antiepileptic drugs with and without cognitive-impairing effects. The results were published in the Journal of the American Geriatrics Society.

The association of antiepileptic drug use with Alzheimer’s disease was assessed in Finnish persons diagnosed with Alzheimer’s disease and their controls without the disease. This study is part of the nationwide register-based MEDALZ study, which includes all 70,718 persons diagnosed with Alzheimer’s disease in Finland during 2005-2011 and their 282,862 controls. The association of antiepileptic drug use with dementia was investigated in a sample from a large German statutory health insurance provider, Allgemeine Ortskrankenkasse (AOK). The dataset includes 20,325 persons diagnosed with dementia in 2004-2011, and their 81,300 controls.

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[WEB SITE] Learning stress-reducing techniques may benefit people with epilepsy

Learning techniques to help manage stress may help people with epilepsy reduce how often they have seizures, according to a study published in the February 14, 2018, online issue of Neurology®, the medical journal of the American Academy of Neurology.

“Despite all the advances we have made with new drugs for epilepsy, at least one-third of people continue to have seizures, so new options are greatly needed,” said study author Sheryl R. Haut, MD, of Montefiore Medical Center and the Albert Einstein College of Medicine in the Bronx, NY, and member of the American Academy of Neurology. “Since stress is the most common seizure trigger reported by patients, research into reducing stress could be valuable.”

The study involved people with seizures that did not respond well to medication. While all of the 66 participants were taking drugs for seizures, all continued to have at least four seizures during about two months before the study started.

During the three-month treatment period all of the participants met with a psychologist for training on a behavioral technique that they were then asked to practice twice a day, following an audio recording. If they had a day where they had signs that they were likely to have a seizure soon, they were asked to practice the technique another time that day. The participants filled out daily electronic diaries on any seizures, their stress level, and other factors such as sleep and mood.

Half of the participants learned the progressive muscle relaxation technique, a stress reduction method where each muscle set is tensed and relaxed, along with breathing techniques. The other participants were the control group-;they took part in a technique called focused attention. They did similar movements as the other group, but without the muscle relaxation, plus other tasks focusing on attention, such as writing down their activities from the day before. The study was conducted in a blinded fashion so that participants and evaluators were not aware of treatment group assignment.

Before the study, the researchers had hypothesized that the people doing the muscle relaxing exercises would show more benefits from the study than the people doing the focused attention exercises, but instead they found that both groups showed a benefit-;and the amount of benefit was the same.

The group doing the muscle relaxing exercises had 29 percent fewer seizures during the study than they did before it started, while the focused attention group had 25 percent fewer seizures, which is not a significant difference, Haut said. She added that study participants were highly motivated as was shown by the nearly 85 percent diary completion rate over a five-month period.

“It’s possible that the control group received some of the benefits of treatment in the same way as the ‘active’ group, since they both met with a psychologist and every day monitored their mood, stress levels and other factors, so they may have been better able to recognize symptoms and respond to stress,” said Haut. “Either way, the study showed that using stress-reducing techniques can be beneficial for people with difficult-to-treat epilepsy, which is good news.”

Haut said more research is needed with larger numbers of people and testing other stress reducing techniques like mindfulness based cognitive therapy to determine how these techniques could help improve quality of life for people with epilepsy.

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[WEB SITE] Findings reveal how seizures can have lasting detrimental effects on memory

October 16, 2017

Although it’s been clear that seizures are linked to memory loss and other cognitive deficits in patients with Alzheimer’s disease, how this happens has been puzzling. In a study published in the journal Nature Medicine, a team of researchers reveals a mechanism that can explain how even relatively infrequent seizures can lead to long-lasting cognitive deficits in animal models. A better understanding of this new mechanism may lead to future strategies to reduce cognitive deficits in Alzheimer’s disease and other conditions associated with seizures, such as epilepsy.

“It’s been hard to reconcile how infrequent seizures can lead to persistent changes in memory in patients with Alzheimer’s disease,” said corresponding author Dr. Jeannie Chin, assistant professor of neuroscience at Baylor College of Medicine. “To solve this puzzle, we worked with a mouse model of Alzheimer’s disease focusing on the genetic changes that seizures might trigger in the memory center of the brain, the hippocampus, that could lead to loss of memory or other cognitive deficits.”

The researchers measured the levels of a number of proteins involved in memory and learning and found that levels of the protein deltaFosB strikingly increase in the hippocampus of Alzheimer’s disease mice that had seizures. DeltaFosB already is well known for its association with other neurological conditions linked to persistent brain activity of specific brain regions, such as addiction. In this study, the researchers found that after a seizure, the deltaFosB protein remains in the hippocampus for an unusually long time; its half-life – the time it takes for the amount of protein to decrease by half – is eight days. Most proteins have a half-life that is between hours and a day or two.

“Interestingly, because deltaFosB is a transcription factor, meaning that its job is to regulate the expression of other proteins, these findings led us to predict that the increased deltaFosB levels might be responsible for suppressing the production of proteins that are necessary for learning and memory,” Chin said. “In fact, we found that when the levels of deltaFosB increase, those of other proteins, such as calbindin, decrease. Calbindin also has been known for a long time to be involved in Alzheimer’s disease and epilepsy, but its mechanism of regulation was not known. We then hypothesized that deltaFosB might be regulating the production of calbindin.”

Further investigations supported the researchers’ hypothesis. The scientists showed that deltaFosB can bind to the gene calbindin suppressing the expression of the protein. When they either prevented deltaFosB activity or experimentally increased calbindin expression in the mice, calbindin levels were restored and the mice improved their memory. And when researchers experimentally increased deltaFosB levels in normal mice, calbindin expression was suppressed and the animals’ memory deteriorated, demonstrating that deltaFosB and calbindin are key regulators of memory.

Connecting pieces of the puzzle

“Our findings have helped us answer the question of how even infrequent seizures can have such lasting detrimental effects on memory,” Chin said. “We found that seizures can increase the levels of deltaFosB in the hippocampus, which results in a decrease in the levels of calbindin, a regulator of memory processes. DeltaFosB has a relatively long half-life, therefore even when seizures are infrequent, deltaFosB remains in the hippocampus for weeks acting like a brake, reducing the production of calbindin and other proteins, and disrupting the consequent brain activity involved in memory. The regulation of gene expression far outlasts the actual seizure event that triggered it.”

The scientists found the same changes in deltaFosB and calbindin levels in the hippocampus of Alzheimer’s disease patients and in the temporal lobe of epilepsy patients. However, they underscore that it is too soon to know whether regulating deltaFosB or calbindin could improve or prevent memory problems or other cognitive deficits in people with Alzheimer’s disease. However, “now that we know that the levels of deltaFosB and calbindin are effective markers of brain activity in the hippocampus and memory function, we propose that these markers could potentially help assess clinical therapies for Alzheimer’s and other diseases with seizures,” Chin said.

Source: Findings reveal how seizures can have lasting detrimental effects on memory

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[WEB SITE] Cannabidiol shows promise to reduce seizures for people with difficult-to-treat epilepsy

Taking cannabidiol may cut seizures in half for some children and adults with Lennox-Gastaut syndrome (LGS), a severe form of epilepsy, according to new information released today from a large scale controlled clinical study that will be presented at the American Academy of Neurology’s 69th Annual Meeting in Boston, April 22 to 28, 2017. Cannabidiol is a molecule from the cannabis plant that does not have the psychoactive properties that create a “high.”

Nearly 40 percent of people with LGS, which starts in childhood, had at least a 50 percent reduction in drop seizures when taking a liquid form of cannabidiol compared to 15 percent taking a placebo.

When someone has a drop seizure, their muscle tone changes, causing them to collapse. Children and adults with LGS have multiple kinds of seizures, including drop seizures and tonic-clonic seizures, which involve loss of consciousness and full-body convulsions. The seizures are hard to control and usually do not respond well to medications. Intellectual development is usually impaired in people with LGS.

Although the drop seizures of LGS are often very brief, they frequently lead to injury and trips to the hospital emergency room, so any reduction in drop seizure frequency is a benefit.

“Our study found that cannabidiol shows great promise in that it may reduce seizures that are otherwise difficult to control,” said study author Anup Patel, MD, of Nationwide Children’s Hospital and The Ohio State University College of Medicine in Columbus and a member of the American Academy of Neurology.

For the randomized, double-blind, placebo-controlled study, researchers followed 225 people with an average age of 16 for 14 weeks. The participants had an average of 85 drop seizures per month, had already tried an average of six epilepsy drugs that did not work for them and were taking an average of three epilepsy drugs during the study.

Participants were given either a higher dose of 20 mg/kg daily cannabidiol, a lower dose of 10 mg/kg daily cannabidiol or placebo as an add-on to their current medications for 14 weeks.

Those taking the higher dose had a 42 percent reduction in drop seizures overall, and for 40 percent, their seizures were reduced by half or more.

Those taking the lower dose had a 37 percent reduction in drop seizures overall, and for 36 percent, seizures were reduced by half or more.

Those taking the placebo had a 17 percent reduction in drop seizures, and for 15 percent, seizures were reduced by half or more.

There were side effects for 94 percent of those taking the higher dose, 84 percent of those taking the lower dose and 72 percent of those taking placebo, but most side effects were reported as mild to moderate. The two most common were decreased appetite and sleepiness.

Those receiving cannabidiol were up to 2.6 times more likely to say their overall condition had improved than those receiving the placebo, with up to 66 percent reporting improvement compared to 44 percent of those receiving the placebo.

“Our results suggest that cannabidiol may be effective for those with Lennox-Gastaut syndrome in treating drop seizures,” said Patel. “This is important because this kind of epilepsy is incredibly difficult to treat. While there were more side effects for those taking cannabidiol, they were mostly well-tolerated. I believe that it may become an important new treatment option for these patients.”

There is currently a plan to submit a New Drug Application to the FDA later this year.

Source: Cannabidiol shows promise to reduce seizures for people with difficult-to-treat epilepsy

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[WEB SITE] tDCS – A Therapy For The Future? – Brain Blogger

Transcranial direct current stimulation (tDCS) is a non-invasive, painless brain stimulation method which uses electrical currents to modulate neuronal activity in specific parts of the brain. A constant, low intensity current is delivered through small electrodes attached to the scalp in order to either increase or reduce neuronal activity.

This is clearly a trending topic: although interest in tDCS dates back to the 1960s, a search in PubMed reveals that more than half of the articles on tDCS were published in the last two years.

Despite numerous studies on different applications for tDCS, its use is still not generally accepted in the clinical setting; tDCS is not an FDA-approved therapy, remaining mostly an experimental method. Although tDCS has been tested on numerous conditions such as depression, anxiety, schizophrenia, Parkinson’s disease, Alzheimer’s disease, chronic pain, fibromyalgia, and stroke, its efficacy is still largely inconclusive.

Many studies applying tDCS have already been published in 2015, as well as a few reviews analyzing its efficacy for different conditions. By gathering the available information for the application of tDSC in a specific context, reviews are particularly useful, allowing researchers to sort through all the conflicting data. And these have actually shown some promising applications for tDSC.

Learning and Memory

There have been claims that tDCS can enhance cognition in healthy adult populations, especially working memory and language production, spiking the interest in tDCS as a neuroenhancement tool.

tDCS seems to act as a neuromodulatory technique, inducing a long-term enhancement or reduction of signal transmission between neurons. By strengthening or weakening neuronal connections, it may facilitate learning and memory formation, as well as neural plasticity that contributes to functional recovery after stroke, for example.

However, a review on the effects of a single-session of tDCS showed that it did not have a significant effect on a variety of cognitive function such as language, episodic memory, working memory or mental arithmetic, just to name a few. Nevertheless, it did not exclude the possibility that tDCS may be effective after multiple sessions.

There are in fact many reports from studies in healthy subjects stating that tDCS enhances verbal performance and learning, improving such outcomes as verbal speed, fluency, and amount of verbal learning. These language enhancement outcomes could potentially be quite useful in treating language deficits associated with different pathological conditions. In fact, tDCS has been used to enhance treatment efficacy in post-stroke aphasia rehabilitation and the results seem promising, with tDCS being effective in increasing language skills despite a high variety of stimulation parameters and patient characteristics.

Language enhancement can also be applied to a word reading context. Repeated tDCS application to adults with developmental dyslexia has been shown to significantly improve reading speed and fluency.

Reports supporting a positive effect on memory enhancement can also be found. Different studies have demonstrated an improvement in working memory and episodic memory in healthy subjects, with an increase in accuracy and in response time. But again, the evidences are still considered insufficient for a clinical application.

These memory enhancement effects could be quite useful in both Alzheimer’s and Parkinson’s disease, and in post-stroke rehabilitation. Again, some promising outcomes in these pathologies have been reported, but there are still conflicting results.

Continue–> tDCS – A Therapy For The Future? | Brain Blogger.

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