Posts Tagged ‘brain’


Prof Sarah Tabrizi , from the UCL Institute of Neurology, led the trials

By James Gallagher

The defect that causes the neurodegenerative disease Huntington’s has been corrected in patients for the first time, the BBC has learned. An experimental drug, injected into spinal fluid, safely lowered levels of toxic proteins in the brain. The research team, at University College London, say there is now hope the deadly disease can be stopped.

Experts say it could be the biggest breakthrough in neurodegenerative diseases for 50 years.

Huntington’s is one of the most devastating diseases. Some patients described it as Parkinson’s, Alzheimer’s and motor neurone disease rolled into one.

Peter Allen, 51, is in the early stages of Huntington’s and took part in the trial: “You end up in almost a vegetative state, it’s a horrible end.”

Huntington’s blights families. Peter has seen his mum Stephanie, uncle Keith and grandmother Olive die from it. Tests show his sister Sandy and brother Frank will develop the disease. The three siblings have eight children – all young adults, each of whom has a 50-50 chance of developing the disease.

The unstoppable death of brain cells in Huntington’s leaves patients in permanent decline, affecting their movement, behaviour, memory and ability to think clearly.

Peter, from Essex, told me: “It’s so difficult to have that degenerative thing in you.

“You know the last day was better than the next one’s going to be.”
Huntington’s generally affects people in their prime – in their 30s and 40s
Patients die around 10 to 20 years after symptoms start
About 8,500 people in the UK have Huntington’s and a further 25,000 will develop it when they are older

Huntington’s is caused by an error in a section of DNA called the huntingtin gene. Normally this contains the instructions for making a protein, called huntingtin, which is vital for brain development. But a genetic error corrupts the protein and turns it into a killer of brain cells.

The treatment is designed to silence the gene.

On the trial, 46 patients had the drug injected into the fluid that bathes the brain and spinal cord. The procedure was carried out at the Leonard Wolfson Experimental Neurology Centre at the National Hospital for Neurology and Neurosurgery in London. Doctors did not know what would happen. One fear was the injections could have caused fatal meningitis. But the first in-human trial showed the drug was safe, well tolerated by patients and crucially reduced the levels of huntingtin in the brain.

Prof Sarah Tabrizi, the lead researcher and director of the Huntington’s Disease Centre at UCL, told the BBC: “I’ve been seeing patients in clinic for nearly 20 years, I’ve seen many of my patients over that time die. For the first time we have the potential, we have the hope, of a therapy that one day may slow or prevent Huntington’s disease . This is of groundbreaking importance for patients and families.”

Doctors are not calling this a cure. They still need vital long-term data to show whether lowering levels of huntingtin will change the course of the disease. The animal research suggests it would. Some motor function even recovered in those experiments.

Peter, Sandy and Frank – as well as their partners Annie, Dermot and Hayley – have always promised their children they will not need to worry about Huntington’s as there will be a treatment in time for them. Peter told the BBC: “I’m the luckiest person in the world to be sitting here on the verge of having that. “Hopefully that will be made available to everybody, to my brothers and sisters and fundamentally my children.”

He, along with the other trial participants, can continue taking the drug as part of the next wave of trials. They will set out to show whether the disease can be slowed, and ultimately prevented, by treating Huntington’s disease carriers before they develop any symptoms.

Prof John Hardy, who was awarded the Breakthrough Prize for his work on Alzheimer’s, told the BBC: “I really think this is, potentially, the biggest breakthrough in neurodegenerative disease in the past 50 years. That sounds like hyperbole – in a year I might be embarrassed by saying that – but that’s how I feel at the moment.”

The UCL scientist, who was not involved in the research, says the same approach might be possible in other neurodegenerative diseases that feature the build-up of toxic proteins in the brain. The protein synuclein is implicated in Parkinson’s while amyloid and tau seem to have a role in dementias.

Off the back of this research, trials are planned using gene-silencing to lower the levels of tau.

Prof Giovanna Mallucci, who discovered the first chemical to prevent the death of brain tissue in any neurodegenerative disease, said the trial was a “tremendous step forward” for patients and there was now “real room for optimism”.

But Prof Mallucci, who is the associate director of UK Dementia Research Institute at the University of Cambridge, cautioned it was still a big leap to expect gene-silencing to work in other neurodegenerative diseases.

She told the BBC: “The case for these is not as clear-cut as for Huntington’s disease, they are more complex and less well understood. But the principle that a gene, any gene affecting disease progression and susceptibility, can be safely modified in this way in humans is very exciting and builds momentum and confidence in pursuing these avenues for potential treatments.”

The full details of the trial will be presented to scientists and published next year.

The therapy was developed by Ionis Pharmaceuticals, which said the drug had “substantially exceeded” expectations, and the licence has now been sold to Roche.

http://www.bbc.com/news/health-42308341

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Last year, doctors of optometry detected more than 320,000 cases of diabetes. Imagine if they could make the same impact when it comes to exposing early signs of Alzheimer’s disease.

November is National Alzheimer’s Disease Awareness Month. An estimated 5.4 million Americans are affected by Alzheimer’s disease, according to the Centers for Disease Control and Prevention (CDC). Projections put the number at 13.8 million by 2050.

Maryke Nijhuis Neiberg, O.D., associate professor in the School of Optometry at Massachusetts College of Pharmacy and Heath Sciences, in Worcester, Massachusetts, considers this an unrealized patient education opportunity for doctors of optometry.

“The earlier diagnoses give doctors and patients a better chance at managing the progressive brain disease and preserving the patient’s quality of life,” Dr. Neiberg says. “There has been some increase in Alzheimer’s awareness over the years, particularly in the eye community, but not enough yet.

“Alzheimer’s is a significant future public health issue,” she adds. “It is still a terminal disease.”

Early intervention

Much of the research on Alzheimer’s disease seeks to slow the disease’s progression. For instance, a study in Biological Psychiatry on Nov. 6 by researchers at the University of Iowa and the University of Texas Southwestern Medical Center in Dallas reports that there may be a new treatment that can slow the depression and cognitive decline associated with Alzheimer’s disease, without affecting amyloid plaque deposits or reactive glia in rats.

Among the early signs of Alzheimer’s, the researchers say, are anxiety, depression and irritability-long before the devastating effects of memory loss.

“Thus, P7C3 compounds may form the basis for a new class of neuroprotective drugs for mitigating the symptoms in patients with Alzheimer’s disease by preserving neuronal cell survival, irrespective of other pathological events,” researchers say. “P7C3 compounds represent a novel route to treating depression, and new-onset depression in elderly patients may herald the development of Alzheimer’s disease with later cognitive impairments to follow.”

Another study in JAMA Ophthalmology in September by researchers at Stanford University and Veterans Affairs Palo Alto Health Care System linked visual impairment and cognition in older adults and also stressed the “potential importance” of vision screening in identifying these patients’ eye disease and cognitive deficits. The AOA strongly recommends comprehensive eye examinations and stresses the limitations of screenings.

Optometry’s role

According to the CDC:

The rate of Alzheimer’s jumped 50 percent between 1999 and 2014.

Americans fear losing their mental capacity more than losing their physical abilities.

More than $230 billion is estimated to be spent in 2017 on providing health care, long-term care, hospice plus unpaid care for relatives with Alzheimer’s and other dementias.

More large-scale research on Alzheimer’s needs to be done, but progress is being made. Dr. Neiberg pointed to research linking optical coherence tomography (OCT) of the macula to Alzheimer’s and Parkinson’s diseases.

“With the advent of OCT, we now know that the retinal ganglion cell layer thins and that the optic nerve cup-to-disc ratio increases in size, not unlike glaucoma,” Dr. Neiberg says. “Alzheimer’s produces visual field defects that are easily confused with glaucoma. What we need is large-scale research to determine how much of the normal tension glaucoma we diagnose and treat is ultimately related to Alzheimer’s disease.”

She adds, “The early perceptual changes that occur in early Alzheimer’s are startling and measurable. One of the earliest signs is a decline in the Benton Visual Retention Test, a test of visual memory. This test requires the duplication of shapes on paper with a pencil, and is scored.

“Research has shown that this test is able to predict high risk for Alzheimer’s 15 years before diagnosis,” she says. “It’s a simple test many developmental and pediatric optometrists already have on their shelves. If we combine that test and the ocular findings we see, we have a very strong indication that something is indeed amiss. Armed with this information, the patient can then consult with their primary care physician, initiate lifestyle modification and request a referral if necessary.”

There is no cure for Alzheimer’s disease. But doctors of optometry can engage patients in conversation about Alzheimer’s disease and how they can manage their own risk factors, including:

Smoking
Mid-life obesity
Sedentary lifestyle
High-cholesterol diet|
Vascular disease (i.e., diabetes and hypertension)

“Lifestyle modification and early access to medication, which can delay the progression of dementia, might be enough to keep the disease at bay for longer,” Dr. Neiberg says. “We should include the Alzheimer’s disease connection when we educate our patients about lifestyle diseases.”

https://finchannel.com/society/health-beauty/69483-doctors-of-optometry-can-spot-early-signs-of-alzheimer-s-disease


The image shows brain tissue from Alzheimer’s rats that were untreated (left) or treated (right) with the neuroprotective compound. The white “holes” indicated by the arrows are areas of brain cell death, and are more numerous in the untreated rats. Although the treatment protects the animals from neuronal cell death and Alzheimer’s-type symptoms, it does not alter the buildup of amyloid plaques and neurofibrillary tangles in the rat brains. The research from the Iowa Neuroscience Institute at the University of Iowa was published online in the journal Biological Psychiatry. Credit: Pieper Lab, University of Iowa.

Treatment with a neuroprotective compound that saves brain cells from dying also prevents the development of depression-like behavior and the later onset of memory and learning problems in a rat model of Alzheimer’s disease. Although the treatment protects the animals from Alzheimer’s-type symptoms, it does not alter the buildup of amyloid plaques and neurofibrillary tangles in the rat brains.

“We have known for a long time that the brains of people with Alzheimer’s disease have amyloid plaques and neurofibrillary tangles of abnormal tau protein, but it isn’t completely understood what is cause or effect in the disease process,” say senior study author Andrew Pieper, MD, PhD, professor of psychiatry in the University of Iowa Carver College of Medicine and associate director of the Iowa Neuroscience Institute at the University of Iowa. “Our study shows that keeping neurons alive in the brain helps animals maintain normal neurologic function, regardless of earlier pathological events in the disease, such as accumulation of amyloid plaque and tau tangles.

Alzheimer’s disease is a devastating neurodegenerative condition that gradually erodes a person’s memory and cognitive abilities. Estimates suggest that more than 5 million Americans are living with Alzheimer’s disease and it is the sixth leading cause of death in the United States, according the National Institute on Aging. In addition to the impact on cognition and memory, Alzheimer’s disease can also affect mood, with many people experiencing depression and anxiety before the cognitive decline is apparent. In fact, people who develop depression for the first time late in life are at a significantly increased risk of developing Alzheimer’s disease.

“Traditional therapies have targeted the characteristic lesions in Alzheimer’s disease, amyloid deposition and tau pathologies. The findings of this study show that simply protecting neurons in Alzheimer’s disease without addressing the earlier pathological events may have potential as a new and exciting therapy,” says Jaymie Voorhees, PhD, first author of the study, which is an article-in-press in Biological Psychiatry.

Saving brain cells protects brain function

Pieper and Voorhees used an experimental compound called P7C3-S243 to prevent brain cells from dying in a rat model of Alzheimer’s disease. The original P7C3 compound was discovered by Pieper and colleagues almost a decade ago, and P7C3-based compounds have since been shown to protect newborn neurons and mature neurons from cell death in animal models of many neurodegenerative diseases, including Parkinson’s disease, amyotrophic lateral sclerosis (ALS), stroke, and traumatic brain injury. P7C3 compounds have also been shown to protect animals from developing depression-like behavior in response to stress-induced killing of nerve cells in the hippocampus, a brain region critical to mood regulation and cognition.

The researchers tested the P7C3 compound in a well-established rat model of Alzheimer’s disease. As these rats age, they develop learning and memory problems that resemble the cognitive impairment seen in people with Alzheimer’s disease. However, the new study revealed another similarity with Alzheimer’s patients. By 15 months of age, before the onset of memory problems, the rats developed depression-like symptoms. Developing depression for the first time late in life is associated with a significantly increased risk for developing Alzheimer’s disease, but this symptom has not been previously seen in animal models of the disease.

Over a three-year period, Voorhees tested a large number of male and female Alzheimer’s and wild type rats that were divided into two groups. One group received the P7C3 compound on a daily basis starting at six months of age, and the other group received a placebo. The rats were tested at 15 months and 24 months of age for depressive-type behavior and learning and memory abilities.

At 15-months of age, all the rats – both Alzheimer’s model and wild type, treated and untreated – had normal learning and memory abilities. However, the untreated Alzheimer’s rats exhibited pronounced depression-type behavior, while the Alzheimer’s rats that had been treated with the neuroprotective P7C3 compound behaved like the control rats and did not show depressive-type behavior.
At 24 months of age (very old for rats), untreated Alzheimer’s rats had learning and memory deficits compared to control rats. In contrast, the P7C3-treated Alzheimer’s rats were protected and had similar cognitive abilities to the control rats.

The team also examined the brains of the rats at the two time points. They found that the traditional hallmarks of Alzheimer’s disease, amyloid plaques, tau tangles, and neuroinflammation, were dramatically increased in the Alzheimer’s rats regardless of whether they were treated with P7C3 or not. However, significantly more neurons survived in the brains of Alzheimer’s rats that had received the P7C3 treatment.

“This suggests a potential clinical benefit from keeping the brain cells alive even in the presence of earlier pathological events in Alzheimer’s disease, such as amyloid accumulation, tau tangles and neuroinflammation,” Pieper says. “In cases of new-onset late life depression, a treatment like P7C3 might be particularly useful as it could help stabilize mood and also protect from later memory problems in patients with Alzheimer’s disease.”

https://medicalxpress.com/news/2017-11-neurons-approach-alzheimer-disease.html

Low-current electrical pulses delivered to a specific brain area during learning improved recollection of distinct memories, according to a study published online in eLife.

Researchers at the University of California, Los Angeles (UCLA) believe electrical stimulation offers hope for the treatment of memory disorders, such as Alzheimer’s disease.

The study involved 13 patients with epilepsy who had ultrafine wires implanted in their brains to pinpoint the origin of seizures. During a person-recognition task, researchers monitored the wires to record neuronal activity as memories were formed, and then sent a specific pattern of quick pulses to the entorhinal area of the brain, an area critical to learning and memory.
In 8 of 9 patients who received electrical pulses to the right side of the entorhinal area, the ability to recognize specific faces and disregard similar-looking ones improved significantly. However, the 4 patients who received electrical stimulation on the left side of the brain area showed no improvement in recall.

By using the ultrafine wires, researchers were able to precisely target the stimulation while using a voltage that was one-tenth to one-fifth of the strength used in previous studies.

“These results suggest that microstimulation with physiologic level currents—a radical departure from commonly used deep brain stimulation protocols—is sufficient to modulate human behavior,” researchers wrote.

The findings also point to the importance of stimulating the right entorhinal region to promote improved memory recollection.

—Jolynn Tumolo

References

Titiz AS, Hill MRH, Mankin EA, et al. Theta-burst microstimulation in the human entorhinal area improves memory specificity. eLife. 2017 October 24.

By Carolyn Gregoire

Long before microdosing was being touted as the Silicon Valley life hack du jour, Dr. James Fadiman was investigating the potential mind-enhancing effects of ingesting psychedelic drugs like LSD and psilocybin, more commonly known as magic mushrooms.

In the 1960s, Fadiman conducted pioneering psychedelic research, including one study in which he gave LSD and another hallucinogen, Mescaline, to scientists, mathematicians and architects to see how it affected creative problem-solving. (His research was one of the last investigations into LSD due to the Food and Drug Administration’s mid-1960s research ban of the substance.)

More recently, Fadiman authored “The Psychedelic Explorer’s Guide,” a how-to manual for safe and therapeutic psychedelic drug experiences.

Now, his research has taken a new turn.

Fadiman is examining the effects of administering psychedelic drugs like LSD and psilocybin in amounts so small that they are below the perceptual threshold. As part of an ongoing research project, Fadiman is collecting the self-reported testimonies of hundreds of people from around the globe who have experimented with psychedelic “microdosing” to treat ailments from anxiety to attention deficit hyperactivity disorder, or simply to improve productivity or break through writer’s block.

How does one microdose? You take a very small dose of either LSD or psilocybin (roughly one-tenth to one-fifth of a normal dose), on a regular schedule. Fadiman recommends dosing in the morning, once every three days. The dose isn’t enough to “trip,” but for some users, it can lead to subtle yet profound internal shifts. Many microdosers report experiencing improvements in mood; enhanced focus, productivity or creativity; less reactivity; and in some cases, even relief from depression or cluster headaches.

“What it seems to do is rebalance people,” Fadiman told The Huffington Post.

HuffPost Science recently sat down with Fadiman to learn more about how microdosing works, and its potential for enhancing well-being and treating a range of health problems.

Where did this idea of microdosing come from?

Dr. Albert Hofmann (the Swiss chemist who discovered LSD) had been microdosing for at least the last couple decades of his life. He lived to be 102 and at age 100 he was still giving two-hour lectures. Hoffman said that he would mainly use it when he was walking in trees, and it would clarify his thinking. So he was the person who first introduced this to many people, and he also said that this was a very under-researched area.

And of course, for thousands of years, indigenous people have been using low doses of mind-altering substances as well.

What types of people are microdosing, and who do you think can benefit most from the practice?

Microdosing seems to improve a vast range of conditions. I’ve explored microdosing as a safer way of doing psychedelics than the high doses that have been used before. Roughly 95 percent of the people who write me have considerable psychedelic experience. I’ll basically tell them, this isn’t going to harm you, let me know what happens.

The general response is that they feel better. There is an actual movement towards increased health or wellness. What that means, for instance, is that people who write in for anxiety seem to get help with their anxiety. People who use it for learning, improve their learning. One Ivy League student said he was using microdosing to get through the hardest math class in the undergraduate curriculum, and he did wonderfully in the class. Another young man used it for severe stuttering, and others have used it for social anxiety. One young woman, an art historian, even found that it regulated her periods and made them painless.

What does your microdosing protocol look like?

On day one, you dose. Day two, you’re still having the effects. Day three, you should be noticeably not having the effects, and on day four you dose again. For self-study, that’s ideal because it gives you a chance to see what’s going on. After a month — which is all I ask of people — most people say that they’re still microdosing, but not as often.

You’ve worked with hundreds of people on a self-reported microdosing study. How did that get started and what have you been finding?

Over the past number of years, people have written to me and said, “I’m interested in microdosing” for this or that reason, “can you help me?” They ask me to tell them what I’ve been suggesting to people, and they ask to be in the study. I then send them a protocol I’ve developed for a self-study and ask them to get back to me. I’ve probably sent out 200 or 300 of these, and I’ve gotten about half as many back as reports. A number are in process right now.

The range of interest goes from “Hey man, new drug, cool” to “I have post-traumatic stress, I’m recovering from cancer, and I hate my meds.” It’s a very wide range. I get a lot of people who say “I have anxiety or depression and I’ve either gotten off my meds or I hate my meds. Could microdosing help?” And my response is, “It’s helped a lot of other people and I hope it helps you. Here’s the protocol.”

I’ve heard there’s potential for enhancing focus and improving symptoms of ADHD, too.

What people basically say is that they’re better. They focus more in class. A number of people have told me that it’s like Adderall but without the side effects. Now these people are coming off Adderall and have used microdosing to help them taper off pharmaceuticals, or at least to take their pharmaceutical use way, way down.

In your study, are you seeing a lot of people turning to microdosing as a way to come off pharmaceuticals?

For some people, it can take a year or two to come off of a pharmaceutical. A number of people have simply said that with microdosing it was much easier. They said they could do it without incredible suffering. A woman who was coming off of some anti-psychotics that she probably should never have been put on said that it wasn’t that she didn’t have the same symptoms, but she didn’t identify with them as much. She said that she could think of her mood swings as her brain chemistry rebalancing.

What’s going on beneath the surface to create these changes?

What microdosing seems to do is rebalance people. Here’s a generalization, which is how I’ve come to this conclusion: A number of people, by the time they’ve finished a month, say, “I’m sleeping better, I’m eating more healthy food, I’ve returned to yoga and I’m doing meditation.” They’ve improved their relationship to their body ― or their body has improved their relationship to them.

One man quit smoking. He said that he knew smoking wasn’t good, and it was as if his body could actually help him make the decision. What seems to happen with microdosing is that you’re more attuned to your own real needs.

Why has there been so little research into microdosing?

There are two main problems. One is that nobody was interested in microdosing, even a couple of years ago. The early research was always high-dose, and the fact that you could take psychedelics as a microdose didn’t occur to people. The only person we knew of who microdosed seriously was Hofmann … It was basically invisible during the time when research was legal and most of the time when it wasn’t.

On the other side of it, I talked with a major researcher who’s done a number of psychedelic studies and who said that he would love to do a microdosing study. I asked him what was stopping him. He said that the Institutional Review Board is not going to say, “Oh you want to give a Schedule I drug to people every few days and have them just go run around?” It’s going to be really hard.

Now, there are two groups, one in Australia and one in Europe, who are starting microdosing studies. I’m working with both of those groups on designing the studies.

https://www.huffingtonpost.com/entry/psychedelic-microdosing-research_us_569525afe4b09dbb4bac9db8

by CHRIS SMYTH

People living in areas with high levels of lithium in tap water are 17 per cent less likely to get dementia, according to a large study that suggests the naturally occurring metal could help to prevent mental decline.

The findings raise the possibility that lithium could one day be added to drinking water to protect the brain in the same way as fluoride is added to protect teeth.

Lithium is already widely available as a psychiatric drug and experts said the findings suggested that it could be used as a treatment to prevent dementia if further trials proved successful. Lithium is known to affect neurological signalling and has long been used as a treatment for conditions such as bipolar disorder. It occurs naturally in water and previous studies have found lower suicide rates in areas with higher levels.

Scientists studied 74,000 older people with dementia and 734,000 without across Denmark, comparing illness rates with lithium levels, which were 15 times higher in some areas.

Scientists at the University of Copenhagen found that dementia rates increased slightly with low levels of lithium before falling sharply above 10 micrograms per litre. At 15 to 27 micrograms/l, dementia rates were 17 per cent lower than for 2-5 micrograms/l, according to results published in JAMA Psychiatry.

The authors acknowledged that other factors could explain the results, including worse healthcare in the remoter areas that had less lithium in water, but they said it was plausible that tiny amounts in tap water could have a significant effect on dementia.

In a linked editorial John McGrath, of the University of Queensland, and Michael Berk, of the University of Melbourne, wrote: “In the spirit of alchemy, could we convert lithium, a simple metal used as a mood stabiliser, into a golden public health intervention that could prevent dementia?

They added: “That a relatively safe, simple, and cheap intervention (ie optimising lithium concentrations in the drinking water) could lead to the primary prevention of dementia is a tantalising prospect.”

David Smith, emeritus professor of pharmacology at the University of Oxford, said the findings tallied with MRI studies showing that lithium salts increased the volume of areas of the brain involved in Alzheimer’s. However, he added: “We should not be adding lithium salts to our tap water because we would not know what amount to use.”

David Reynolds, chief scientific officer at Alzheimer’s Research UK, said: “It is potentially exciting that low doses of a drug already available in the clinic could help limit the number of people who develop dementia.”

Rob Howard, professor of old-age psychiatry at University College London, said: “These results represent another important piece of evidence for lithium’s potential as a treatment for Alzheimer’s disease. We now need clinical trials of lithium in patients with Alzheimer’s disease to determine once and for all whether this cheap and well-tolerated element can slow dementia progression.”

http://www.theaustralian.com.au/news/world/the-times/lithium-in-tap-water-could-lower-dementia-risk/news-story/c40599203eca195402c03c0a168961a6

Meet Helen Lavretsky, Professor of Psychiatry at UCLA, recently completed a pilot study of Kundalini yoga vs memory training in older adults with subjective memory complaints and mild cognitive impairment.

Patients assigned to yoga practice for 12 weeks with daily meditation for 12 minutes in weekly one hour classes did better than those who participated in memory training classes in verbal and visual memory, executive function, mood resilience, anxiety, and connectivity of the brain.

Results suggest that yoga can be a cognitive enhancement or brain fitness exercise that can confer similar or even more extensive cognitive resilience than memory training—the gold standard—in older adults.

Meditation in this study was practiced with music recorded on the White Sun album, which received a Grammy award this year.

Dr Lavretsky is Professor of Psychiatry at UCLA. She also directs the Late Life Mood, Stress, and Wellness Research Program at the Semel Institute at UCLA.

http://www.psychiatrictimes.com/geriatric-psychiatry/cognitive-enhancement-with-yoga?GUID=C523B8FD-3416-4DAC-8E3C-6E28DE36C515&rememberme=1&ts=17082017

Eyre HA1, Siddarth P1, Acevedo B1, et al. A randomized controlled trial of Kundalini yoga in mild cognitive impairment. Int Psychogeriatr. 2017;29:557-567. https://www.cambridge.org/core/journals/international-psychogeriatrics/article/randomized-controlled-trial-of-kundalini-yoga-in-mild-cognitive-impairment/138A3EB97520CE72B01D17059B7AA286.

Yang H, Leaver AM, Siddarth P, et al. Neurochemical and Neuroanatomical Plasticity Following Memory Training and Yoga Interventions in Older Adults with Mild Cognitive Impairment. Front Aging Neurosci. 2016;8:277. eCollection 2016. http://journal.frontiersin.org/article/10.3389/fnagi.2016.00277/full.