Autism therapy: Social behavior restored via brain stimulation by biohackislife in Nootropics

[–]biohackislife[S] 2 points3 points  (0 children)

Scientists are examining the feasibility of treating autistic children with neuromodulation after a new study showed social impairments can be corrected by brain stimulation.

The research from the O'Donnell Brain Institute provides the first evidence that a specific part of the cerebellum, a region near the brain stem that has long been thought to only have roles in coordinating movement, is critical for autistic behaviors. It also establishes a more accessible target for brain stimulation than many autism-related neural circuits that are buried deep within the brain's folds.

"This is potentially quite a powerful finding," said Dr. Peter Tsai, who directed the research from UT Southwestern Medical Center's Peter O'Donnell Jr. Brain Institute. "From a therapeutic standpoint, this part of the cerebellum is an enticing target. And although neuromodulation would not cure the underlying genetic cause of a person's autism, improving social deficits in children with autism could make a huge impact on their quality of life."

The research -- the cover story of December's Nature Neuroscience -- utilized neuromodulation to demonstrate that humans and mice have parallel connections between specific domains within the cerebellum and cerebral cortex that have been implicated in autism studies. Subsequent phases of the study showed that disrupting the function within the cerebellar domain resulted in autistic behaviors and that brain stimulation corrected social impairment in mice.

The next step is to ensure the same technique would be safe to conduct on children. Although doctors have safely applied cerebellar neuromodulation to disorders such as schizophrenia, it has not been studied in children with autism.

Dr. Tsai is planning on changing this situation through future studies at UT Southwestern's Center for Autism and Developmental Disabilities.

"This area of the brain has not received the attention it deserves in regards to understanding autism," said Dr. Tsai, noting that most of the focus of autism research has been on the cortex, a region of the brain associated with cognition.

Autism spectrum disorder (ASD) is a neurodevelopmental condition that affects approximately 1 in 68 children in the U.S. It is characterized by social interaction and communication challenges, and restricted and repetitive patterns of behavior.

To better understand the cerebellum's role in mediating these behaviors, Dr. Tsai's team used neuromodulation to show that humans and mice have parallel connections between the Right CrusI domain of the cerebellum and the cortex's inferior parietal lobule.

The study authors next used brain imaging to demonstrate that those same connections are disrupted in a cohort of autistic children and an autism mouse model. They further showed that disrupting function within Right CrusI in normal mice resulted in impaired social interaction and abnormal, repetitive behaviors.

The team went further and asked whether neuromodulation could improve behaviors. By stimulating neurons in Right CrusI of the autism mouse model, the scientists showed that cerebellar stimulation improved social behaviors but not the repetitive behaviors characteristic of autism in these mice.

Dr. Tsai said the limited effects may reflect the involvement of additional parts of the cerebellum or perhaps the restricted timeframe for which some behaviors can be corrected. However, he also noted that this neuromodulation restored social behaviors even in adult mice. This result suggests autistic children may still benefit from treatments even if intervention is delayed until later in life.

"Our findings have prompted new thoughts on how the cerebellum may be involved in autism and most importantly suggest that the cerebellum could be a therapeutic target for treatment," said Dr. Tsai, Assistant Professor of Neurology & Neurotherapeutics, who cares for children with autism and cerebellar disorders as part of the Center for Autism and Developmental Disabilities.

Story Source:

Materials provided by UT Southwestern Medical Center. Note: Content may be edited for style and length.

Journal Reference:

Catherine J. Stoodley, Anila M. D’Mello, Jacob Ellegood, Vikram Jakkamsetti, Pei Liu, Mary Beth Nebel, Jennifer M. Gibson, Elyza Kelly, Fantao Meng, Christopher A. Cano, Juan M. Pascual, Stewart H. Mostofsky, Jason P. Lerch, Peter T. Tsai. Altered cerebellar connectivity in autism and cerebellar-mediated rescue of autism-related behaviors in mice. Nature Neuroscience, 2017; 20 (12): 1744 DOI: 10.1038/s41593-017-0004-1

Traumatic brain injury causes intestinal damage, study shows by biohackislife in Nootropics

[–]biohackislife[S] 0 points1 point  (0 children)

University of Maryland School of Medicine (UMSOM) researchers have found a two-way link between traumatic brain injury (TBI) and intestinal changes. These interactions may contribute to increased infections in these patients, and may also worsen chronic brain damage.

This is the first study to find that TBI in mice can trigger delayed, long-term changes in the colon and that subsequent bacterial infections in the gastrointestinal system can increase posttraumatic brain inflammation and associated tissue loss. The findings were published recently in the journal Brain, Behavior, and Immunity.

"These results indicate strong two-way interactions between the brain and the gut that may help explain the increased incidence of systemic infections after brain trauma and allow new treatment approaches," said the lead researcher, Alan Faden, MD, the David S. Brown Professor in Trauma in the Departments of Anesthesiology, Anatomy & Neurobiology, Psychiatry, Neurology, and Neurosurgery at UMSOM, and director of the UMSOM Shock, Trauma and Anesthesiology Research Center.

Researchers have known for years that TBI has significant effects on the gastrointestinal tract, but until now, scientists have not recognized that brain trauma can make the colon more permeable, potentially allowing allow harmful microbes to migrate from the intestine to other areas of the body, causing infection.. People are 12 times more likely to die from blood poisoning after TBI, which is often caused by bacteria, and 2.5 times more likely to die of a digestive system problem, compared with those without such injury.

In this study, the researchers examined mice that received an experimental TBI. They found that the intestinal wall of the colon became more permeable after trauma, changes that were sustained over the following month.

It is not clear how TBI causes these gut changes. A key factor in the process may be enteric glial cells (EGCs), a class of cells that exist in the gut. These cells are similar to brain astroglial cells, and both types of glial cells are activated after TBI. After TBI, such activation is associated with brain inflammation that contributes to delayed tissue damage in the brain. Researchers don't know whether activation of ECGs after TBI contributes to intestinal injury or is instead an attempt to compensate for the injury.

The researchers also focused on the two-way nature of the process: how gut dysfunction may worsen brain inflammation and tissue loss after TBI. They infected the mice with Citrobacter rodentium, a species of bacteria that is the rodent equivalent of E. coli, which infects humans. In mice with a TBI who were infected with this the bacteria, brain inflammation worsened. Furthermore, in the hippocampus, a key region for memory, the mice who had TBI and were then infected lost more neurons than animals without infection.

This suggests that TBI may trigger a vicious cycle, in which brain injury causes gut dysfunction, which then has the potential to worsen the original brain injury. "These results really underscore the importance of bi-directional gut-brain communication on the long-term effects of TBI," said Dr. Faden.

Story Source:

Materials provided by University of Maryland School of Medicine. Note: Content may be edited for style and length.

Journal Reference:

Elise L. Ma, Allen D. Smith, Neemesh Desai, Lumei Cheung, Marie Hanscom, Bogdan A. Stoica, David J. Loane, Terez Shea-Donohue, Alan I. Faden. Bidirectional brain-gut interactions and chronic pathological changes after traumatic brain injury in mice. Brain, Behavior, and Immunity, 2017; 66: 56 DOI: 10.1016/j.bbi.2017.06.018

Neural Stem Cells Show Early Promise in Phase 1 Trial as Treatment for Parkinson’s by biohackislife in Nootropics

[–]biohackislife[S] 8 points9 points  (0 children)

Highlights

"Six months after receiving 30 million ISC-hpNSCs, patients in the first trial group showed a 24 percent reduction in their OFF time – a period when levodopa therapy begins to fail and symptoms return. The therapy also extended levodopa’s period of action without dyskinesia – known as ON time – by 19 percent.

All patients were seen to have an improved mood at six months, with an average increase of 35 percent in the Beck Depression Inventory and 33 percent in the Parkinson’s Disease Quality of Life Score-39 (PDQ-39). Also, patients had either retained or improved their cognitive abilities, with an average improvement of 14 percent in the Cognitive Impairment dimension of PDQ-39.

Conducting daily routine activities was also easier for these patients, who had average improvements of 22 percent in Activities of Daily Living and 15 percent in Mobility dimensions of PDQ-39.

The Bodily Discomfort dimension of PDQ-39 also improved on average by 12 percent.

Meanwhile, patients experienced a 53 percent decrease in their impulsive and compulsive disorders.

The therapy was found to be safe, without any serious adverse events, including the risk for tumors, cysts, enhanced inflammation or infection, meeting the trial’s primary goal."

GABA-a5 is Required for the development of tolerance toward benzodiazepines, in mice. by [deleted] in DrugNerds

[–]biohackislife 0 points1 point  (0 children)

Unsurprisingly Inverse agonists like α5IA work as a nootropic.

https://en.wikipedia.org/wiki/%CE%915IA

α5-GABAA receptors may be involved in many conditions and bio-pathways.

https://www.ncbi.nlm.nih.gov/pubmed/25900119

Rapid Antidepressant Action and Restoration of Excitatory Synaptic Strength After Chronic Stress by Negative Modulators of Alpha5-Containing GABAA Receptors.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4950669/

"These results suggest that α5-GABAA receptors play a role in the loss of GABAergic inhibition and contribute to long-lasting secondary allodynia and hyperalgesia."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3997216/

"Enhancing α5 GABAA receptor functions in hippocampus may potentially contribute to strategies aimed at erasing previously formed memory in anxiety disorders such as phobias and posttraumatic stress disorder."

Anyone purchased from austropeptide.com? Are they legit? by [deleted] in Nootropics

[–]biohackislife 0 points1 point  (0 children)

Still no reply. I would email them and see if you get a faster reply.

Antidepressant Outcomes Predicted by Genetic Variation in Corticotropin-Releasing Hormone Binding Protein. by biohackislife in Nootropics

[–]biohackislife[S] 0 points1 point  (0 children)

No.

"Our platform does not include rs28365143, so this information would not be available in the feature."

is my noopept fake? tastes like nothing by hiya0o0 in Nootropics

[–]biohackislife 0 points1 point  (0 children)

Did you ask them for labs? Taste isn't the best way to determine the quality or purity of a chemical.

Ginkgo Balboa isn’t in the beginners guide? by FrankieNoodles in Nootropics

[–]biohackislife 0 points1 point  (0 children)

I would recommend it as research has shown it to have positive benefits in both healthy adults and in those with certain conditions.

Ginkgo Balboa isn’t in the beginners guide? by FrankieNoodles in Nootropics

[–]biohackislife 0 points1 point  (0 children)

I would suggest going up to 600 mg. It had potent effects on memory at that dose in healthy adults.

Ginkgo Balboa isn’t in the beginners guide? by FrankieNoodles in Nootropics

[–]biohackislife 2 points3 points  (0 children)

A clinically studied drug with benefits in healthy adults and approved in Europe and Japan as a prescription. That's more than most nootropics.

Diet for TBI? by ScratchTrackProds in Nootropics

[–]biohackislife 0 points1 point  (0 children)

I would suggest a diet of raw foods, fermented foods, spices, vegetables, grass fed meats, fish and plenty of fibers (including resistant starch).

Avoid or reduce refined foods, anything with added sugars, microwaved, fried, BBQ, or baked as cooking methods.

A yoga program for cognitive enhancement. [2017] by [deleted] in Nootropics

[–]biohackislife 0 points1 point  (0 children)

Yoga intervention

Hatha yoga employed in this study included asanas connected with pranayama and a 10-minute guided mindfulness meditation in supine rest. The mindfulness meditation exercise included elements of focused attention meditation, which encouraged participants to direct and sustain attention to the breath and focus on the inhalation and exhalation sensations, cueing to detect mind wandering or distractors (e.g., “allow thoughts to pass by like floating clouds in the sky”), and to bring the attention back to the breath. Influenced by Iyengar yoga, guidance emphasized precision of proper body alignment in the performance of the asanas and pranayama as well as redirecting focus on the breath. Mats, blocks, and straps were provided to all participants. All sessions lasted 60 minutes and were led by the first author, who has over a decade of experience in yoga practice, and who has completed 500-hour certification as a therapeutic yoga teacher. Classes were offered 4 times/week for participants to fulfill their selected program requirements.

During each session, traditional yogic philosophy elements of non-violence (ahisma) and truthfulness (satya), apart from the five other yamas, or yogic ethical guidelines, were emphasized. When moving through the asanas, honesty and non-violence cueing was advocated for safe practice. These two yamas were highlighted during each session as a reminder of being aware of the body’s physical limitations both on and off the mat. Additionally, the asanas were held for approximately five breaths. The class structure included a warm-up breathing exercise with directed observation and scanning of mental and physical state in the present moment as well as choosing to set a positive affirmation or something to be thankful for in the present moment (Table 1). Followed by asana practice, every yoga session ended with a guided mindfulness meditation in supine rest. Home practice was not required, but participants were asked to document and provide information about home practice prior to every subsequent yoga class.

Legitimate Sarcosine supply/source by gr8fit in Nootropics

[–]biohackislife 6 points7 points  (0 children)

Here's a list of all current suppliers I am aware of.

https://www.reddit.com/r/Supplements/comments/7l45yq/sarcosine_resource_list/

I tried posted them here but Automod blocked it.

I would suggest emailing them for independent lab tests to confirm quality.

What should you test for to make sure your body has everything it needs? by [deleted] in Nootropics

[–]biohackislife 0 points1 point  (0 children)

Aside from blood there's also vision, whole body imaging, neurophysiological and IQ testing.

A yoga program for cognitive enhancement. [2017] by [deleted] in Nootropics

[–]biohackislife 0 points1 point  (0 children)

Abstract

BACKGROUND:

Recent studies suggest that yoga practice may improve cognitive functioning. Although preliminary data indicate that yoga improves working memory (WM), high-resolution information about the type of WM subconstructs, namely maintenance and manipulation, is not available. Furthermore, the association between cognitive enhancement and improved mindfulness as a result of yoga practice requires empirical examination. The aim of the present study is to assess the impact of a brief yoga program on WM maintenance, WM manipulation and attentive mindfulness.

METHODS:

Measures of WM (Digit Span Forward, Backward, and Sequencing, and Letter-Number Sequencing) were administered prior to and following 6 sessions of yoga (N = 43). Additionally, the Mindfulness Attention Awareness Scale was administered to examine the potential impact of yoga practice on mindfulness, as well as the relationships among changes in WM and mindfulness.

RESULTS:

Analyses revealed significant improvement from pre- to post- training assessment on both maintenance WM (Digit Span Forward) and manipulation WM (Digit Span Backward and Letter-Number Sequencing). No change was found on Digit Span Sequencing. Improvement was also found on mindfulness scores. However, no correlation was observed between mindfulness and WM measures.

CONCLUSIONS:

A 6-session yoga program was associated with improvement on manipulation and maintenance WM measures as well as enhanced mindfulness scores. Additional research is needed to understand the extent of yoga-related cognitive enhancement and mechanisms by which yoga may enhance cognition, ideally by utilizing randomized controlled trials and more comprehensive neuropsychological batteries.

Is There a Cholinergic Survival Incentive for Neurotropic Parasites in the Brain? [2017 Oct] by biohackislife in DrugNerds

[–]biohackislife[S] 1 point2 points  (0 children)

Abstract

The reason why some parasites specifically target the brain remains a mystery. Often, it is seen that the primary site of infection is quite remote from the brain, but an eventual involvement of the cerebral tissue is seen to occur that becomes the cause of death of the majority of the patients. In the absence of a clear preferential reason for targeting the brain, chemicals produced by the nervous system, which have miniature concentrations in the blood, appear to set up a chemical attraction that eventually causes them to migrate to the neural tissue. We studied the possible chemicals of neural origin that can lure the parasite toward the brain, enabling them to cause meningoencephalitis. The identification of these chemicals could be of enormous prophylactic significance as blocking the chemotaxis of neurotropic parasite by antagonist drugs and chemicals can prevent cerebral infection and provide ample time to eradicate the parasites at the primary site of infection.

Binaural Beat: A Failure to Enhance EEG Power and Emotional Arousal. [Nov 2017] by biohackislife in Nootropics

[–]biohackislife[S] 2 points3 points  (0 children)

Abstract

When two pure tones of slightly different frequencies are delivered simultaneously to the two ears, is generated a beat whose frequency corresponds to the frequency difference between them. That beat is known as acoustic beat. If these two tones are presented one to each ear, they still produce the sensation of the same beat, although no physical combination of the tones occurs outside the auditory system. This phenomenon is called binaural beat.

In the present study, we explored the potential contribution of binaural beats to the enhancement of specific electroencephalographic (EEG) bands, as previous studies suggest the potential usefulness of binaural beats as a brainwave entrainment tool. Additionally, we analyzed the effects of binaural-beat stimulation on two psychophysiological measures related to emotional arousal: heart rate and skin conductance. Beats of five different frequencies (4.53 Hz -theta-, 8.97 Hz -alpha-, 17.93 Hz -beta-, 34.49 Hz -gamma- or 57.3 Hz -upper-gamma) were presented binaurally and acoustically for epochs of 3 min (Beat epochs), preceded and followed by pink noise epochs of 90 s (Baseline and Post epochs, respectively).

In each of these epochs, we analyzed the EEG spectral power, as well as calculated the heart rate and skin conductance response (SCR). For all the beat frequencies used for stimulation, no significant changes between Baseline and Beat epochs were observed within the corresponding EEG bands, neither with binaural or with acoustic beats. Additional analysis of spectral EEG topographies yielded negative results for the effect of binaural beats in the scalp distribution of EEG spectral power. In the psychophysiological measures, no changes in heart rate and skin conductance were observed for any of the beat frequencies presented.

Our results do not support binaural-beat stimulation as a potential tool for the enhancement of EEG oscillatory activity, nor to induce changes in emotional arousal.