Brain

Brain

A Link Between Gut Bacteria and Neurogenesis: Mouse Study

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I shared here many times that प्राण is cellular intelligence and memory. Mar the प्राण, do not retain प्राण and your body cells lose intelligence.

Lost cellular intelligence = Zombie cells = Prone to proliferation, inflammation, retard responses.

Here is the paper in support of this observation.

antibiotics = lack of prana = brain development hampered = memory function impaired.


Research


A Link Between Gut Bacteria and Neurogenesis: Mouse Study

Summary: According to a new mouse study, antibotics that are strong enough to kill gut bacteria can also halt the growth of hippocampal neurons.

Source: Cell Press.

http://neurosciencenews.com/neurogenesis-gut-bacteria-4253/

http://www.cell.com/cell-reports/pdf/S2211-1247(16)30518-6.pdf

Antibiotics strong enough to kill off gut bacteria can also stop the growth of new brain cells in the hippocampus, a section of the brain associated with memory, reports a study in mice published May 19 in Cell Reports. Researchers also uncovered a clue to why– a type of white blood cell seems to act as a communicator between the brain, the immune system, and the gut.

“We found prolonged antibiotic treatment might impact brain function,” says senior author Susanne Asu Wolf of the Max-Delbrueck-Center for Molecular Medicine in Berlin, Germany. “But probiotics and exercise can balance brain plasticity and should be considered as a real treatment option.”

Wolf first saw clues that the immune system could influence the health and growth of brain cells through research into T cells nearly 10 years ago. But there were few studies that found a link from the brain to the immune system and back to the gut.

In the new study, the researchers gave a group of mice enough antibiotics for them to become nearly free of intestinal microbes. Compared to untreated mice, the mice who lost their healthy gut bacteria performed worse in memory tests and showed a loss of neurogenesis (new brain cells) in a section of their hippocampus that typically produces new brain cells throughout an individual’s lifetime. At the same time that the mice experienced memory and neurogenesis loss, the research team detected a lower level of white blood cells (specifically monocytes) marked with Ly6Chi in the brain, blood, and bone marrow. So researchers tested whether it was indeed the Ly6Chi monocytes behind the changes in neurogenesis and memory.

In another experiment, the research team compared untreated mice to mice that had healthy gut bacteria levels but low levels of Ly6Chi either due to genetics or due to treatment with antibodies that target Ly6Chi cells. In both cases, mice with low Ly6Chi levels showed the same memory and neurogenesis deficits as mice in the other experiment who had lost gut bacteria. Furthermore, if the researchers replaced the Ly6Chi levels in mice treated with antibiotics, then memory and neurogenesis improved.

“For us it was impressive to find these Ly6Chi cells that travel from the periphery to the brain, and if there’s something wrong in the microbiome, Ly6Chi acts as a communicating cell,” says Wolf.

Researchers connect brain blood vessel lesions to intestinal bacteria

https://www.ninds.nih.gov/News-Events/News-and-Press-Releases/Press-Releases/Researchers-connect-brain-blood-vessel-lesions

A study in mice and humans suggests that bacteria in the gut can influence the structure of the brain’s blood vessels, and may be responsible for producing malformations that can lead to stroke or epilepsy. The research, published in Nature, adds to an emerging picture that connects intestinal microbes and disorders of the nervous system. The study was funded by the National Institute of Neurological Disorders and Stroke (NINDS), a part of the National Institutes of Health (NIH).

Cerebral cavernous malformations (CCMs) are clusters of dilated, thin-walled blood vessels that can lead to seizures or stroke when blood leaks into the surrounding brain tissue. A team of scientists at the University of Pennsylvania investigated the mechanisms that cause CCM lesions to form in genetically engineered mice and discovered an unexpected link to bacteria in the gut. When bacteria were eliminated the number of lesions was greatly diminished.

“This study is exciting because it shows that changes within the body can affect the progression of a disorder caused by a genetic mutation,” said Jim I. Koenig, Ph.D., program director at NINDS.

High-Fat Junk diet, Kids and Brain development

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HIGH FAT DIET =>> REDUCED GLUCOSE for BRAIN ==> Slow Learning and impaired memory.

How high fat junk diet reduces potential of your brain to support mind? And in turn, shape you as future moron.

A high-fat diet of three days in mice leads to a reduction in the amount of glucose that reaches the brain.

High-fat-content foods throw our bodies out of kilter. Obesity and diseases such as type 2 diabetes can be the result. But what does a high-fat diet actually do to our brain? Scientists from the Max Planck Institute for Metabolism Research in Cologne have looked into the brains of mice to understand how obesity and diabetes develop.


Research


Myeloid-Cell-Derived VEGF Maintains Brain Glucose Uptake and Limits Cognitive Impairment in Obesity

http://www.cell.com/cell/abstract/S0092-8674(16)30331-2

“A high-fat diet reduces the uptake of blood glucose into the brain in as little as three days. So the brain is starving, even though the mice are consuming a lot of calories daily. Responsible for this is the protein GLUT-1, which is the most important glucose transporter at the blood-brain barrier,” explained Alexander Jais, author of the study. Possible triggers for the reduction of the GLUT-1 transporter are free saturated fatty acids that have a toxic effect on the cells of the blood-brain barrier. The brain lacks glucose in significant areas: the hypothalamus, which controls metabolism, and the cerebral cortex, responsible for learning and memory.

Highlights

  • Acute high-fat feeding suppresses GLUT1 expression at the blood-brain barrier (BBB)
  • Macrophages at the BBB increase VEGF expression upon prolonged HFD feeding
  • Inducible GLUT1 deletion in brain endothelial cells leads to increased VEGF secretion
  • Myeloid-cell-specific disruption of VEGF impairs cognitive function in obesity

Summary

High-fat diet (HFD) feeding induces rapid reprogramming of systemic metabolism. Here, we demonstrate that HFD feeding of mice downregulates glucose transporter (GLUT)-1 expression in blood-brain barrier (BBB) vascular endothelial cells (BECs) and reduces brain glucose uptake. Upon prolonged HFD feeding, GLUT1 expression is restored, which is paralleled by increased expression of vascular endothelial growth factor (VEGF) in macrophages at the BBB. In turn, inducible reduction of GLUT1 expression specifically in BECs reduces brain glucose uptake and increases VEGF serum concentrations in lean mice. Conversely, myeloid-cell-specific deletion of VEGF in VEGFΔmyel mice impairs BBB-GLUT1 expression, brain glucose uptake, and memory formation in obese, but not in lean mice. Moreover, obese VEGFΔmyel mice exhibit exaggerated progression of cognitive decline and neuroinflammation on an Alzheimer’s disease background. These experiments reveal that transient, HFD-elicited reduction of brain glucose uptake initiates a compensatory increase of VEGF production and assign obesity-associated macrophage activation a homeostatic role to restore cerebral glucose metabolism, preserve cognitive function, and limit neurodegeneration in obesity.

Rural serenity : Innate urge, hard-wired

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Reason why so many resorts, restaurants, spiritual shops with rustic look run the business with handsome profit. Of course by exploiting our hard wired instinct.

Eternal urge to live life with mother.

urban-vs-rural


Research


Human brain hard-wired for rural tranquillity

Humans may be hard-wired to feel at peace in the countryside and confused in cities – even if they were born and raised in an urban area.

“When looking at urban environments the brain is doing a lot of processing because it doesn’t know what this environment is,” he said. “The brain doesn’t have an immediate natural response to it, so it has to get busy. Part of the brain that deals with visual complexity lights up: ‘What is this that I’m looking at?’ Even if you have lived in a city all your life, it seems your brain doesn’t quite know what to do with this information and has to do visual processing,” he said.

Rural images produced a “much quieter” response in a “completely different part of the brain”, he added. “There’s much less activity. It seems to be in the limbic system, a much older, evolutionarily, part of the brain that we share with monkeys and primates.”

“I think we have neglected the relationship that human beings have with their environment and we are strongly connected to it,” he said. “If you don’t get the conditions right in zoos, the animals start behaving in a wacky way. There have been studies done with laboratory animals showing their feeding is abnormal. Sometimes they stop eating and sometimes they eat excessively. How far we can draw that parallel, I don’t know.”

http://www.independent.co.uk/news/science/human-brain-hard-wired-for-rural-tranquillity-8996368.html

Pain killer/Antibiotics promotes प्रज्ञा अपराध (Intellectual Errors)

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PainKillers

We noted in this note that प्रज्ञा अपराध – The crime of injecting intellectual errors in day to day decision making – Root cause of all ill-health issues.

Impaired Intellect + Impaired self-control + Impaired memory = High chances of प्रज्ञा अपराध (misuse or no use of human brain/mind)

प्रज्ञापराधो हि मूलं रोगाणाम् |

प्रज्ञापराध कुछ और नहीं, बल्कि प्रकृति के नियमों की अवहेलना है।व्यक्ति जब जीवन के समग्र रूप को भूल खुद को इससे अलग मानने लगता है, तब वह प्रज्ञापराध का दोषी हो जाता है।

अनेक ग्रंथों में कहा गया है कि शरीर की रोगों से रक्षा करना मनुष्य का प्रमुख कर्तव्य है। पर कई बार तमाम कोशिशों के बाद भी बीमारियां हमें अपना शिकार बना ही लेती हैं। आखिर क्यों होते हैं रोग? इस बारे में आयुर्वेद कहता है कि प्रज्ञापराध ही हर रोग की जड़ है। प्रज्ञापराध दो शब्दों से मिल कर बना है: प्रज्ञा और अपराध। प्रज्ञा का अर्थ है ज्ञान और अपराध का अर्थ है गलत कार्य। जानकारी होने के बावजूद गलत काम करना, उपेक्षा या अवहेलना करना ही प्रज्ञापराध है। आयुर्वेद में कहा गया है कि प्रज्ञापराध को महामारियों का प्रमुख कारण माना जा सकता है। जानकारी होने के बावजूद किए जाने वाले इस प्रकार के अपराधों को तीन श्रेणियों में बांटा जाता है। पहले प्रकार का अपराध है किसी नियम की उपेक्षा करना। दूसरे प्रकार के अपराध वे हैं, जिनके नुकसान हम जानते हैं, फिर भी हम वे काम करते हैं। जैसे कि सिगरेट पीना। कोई व्यक्ति कमजोर इच्छा शक्ति के कारण सिगरेट पीना नहीं छोड़ पाता है, तो वह अपने प्रति अपराध करता है। तीसरे प्रकार के अपराध वे हैं, जो हम ज्ञान अथवा स्मृति के अभाव में कर बैठते हैं।

http://hindi.speakingtree.in/article/content-247515

It is state of intellect that cannot decide what is favorable and what is not based on individual’s current state of mind and body.

Our education system does not train us to avoid these crimes. Parenting? They don’t have time. Society? It is no more a live entity.

Only way to improve health of society is to train society to avoid प्रज्ञा अपराध.

On the other hand, modern medicines , with a motive to hide the real symptoms, give such medicines that promote intellectual errors!


Research


This popular painkiller may hamper your ability to notice errors, U of T researchers say

https://www.utoronto.ca/news/popular-painkiller-may-hamper-your-ability-notice-errors-u-t-researchers-say

Cognitive control is an important neurological function because people are constantly doing cognitive tasks that flow automatically like reading, walking or talking. These tasks require very little cognitive control because they are well mapped out neurological processes, notes Randles.

“Sometimes you need to interrupt your normal processes or they’ll lead to a mistake, like when you’re talking to a friend while crossing the street, you should still be ready to react to an erratic driver,” explains Randles.

“The task we designed is meant to capture that since most of the stimuli were Go, so you end up getting into a routine of automatically hitting the Go button. When you see a No Go, that requires cognitive control because you need to interrupt the process.”

The study was double blind, so neither the researcher running the study nor the participant knew whether they had been given a placebo or acetaminophen.

An unexpected and surprise finding that Randles plans to explore more closely is that those who received an acetaminophen dose appeared to miss more of the Go stimuli than they should have. He plans on expanding on the error detection aspect of the research to see whether acetaminophen is possibly causing people to “mind wander” and become distracted.

“An obvious question is if people aren’t detecting these errors, are they also making errors more often when taking acetaminophen? This is the first study to address this question, so we need more work and ideally with tasks more closely related to normal daily behaviour.”

Evidence Suggests Early Exposure to Antibiotics Might Lead to Long-Term Behavioural Changes

Low-dose penicillin in early life induces long-term changes in murine gut microbiota, brain cytokines and behavior

There is increasing concern about potential long-term effects of antibiotics on children’s health. Epidemiological studies have revealed that early-life antibiotic exposure can increase the risk of developing immune and metabolic diseases, and rodent studies have shown that administration of high doses of antibiotics has long-term effects on brain neurochemistry and behaviour. Here we investigate whether low-dose penicillin in late pregnancy and early postnatal life induces long-term effects in the offspring of mice. We find that penicillin has lasting effects in both sexes on gut microbiota, increases cytokine expression in frontal cortex, modifies blood–brain barrier integrity and alters behaviour. The antibiotic-treated mice exhibit impaired anxiety-like and social behaviours, and display aggression. Concurrent supplementation with Lactobacillus rhamnosus JB-1 prevents some of these alterations. These results warrant further studies on the potential role of early-life antibiotic use in the development of neuropsychiatric disorders, and the possible attenuation of these by beneficial bacteria.

http://www.nature.com/articles/ncomms15062

Long Term Memory and Mind

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Our text books teaches us that the brain is where memories are stored. Brain is where thoughts take birth. Brain is where decisions are taken. Reductionist science. Poor ignorance.

This experiment on Aplysia, a sea slugs shows something else. Brain plays a role of platform to execute the actions, memories, decisions and does not store in brain.

Researchers trained these creatures to respond to certain neurotransmitter signals. They then used chemicals to return the synapses to their pre-trained state, which basically eliminated the memorized reflexes. But even though the researchers had altered the neural connections, they found that the long-term memories for those reflexes still persisted covertly. According to the authors of the paper, “these results challenge the idea that stable synapses store long-term memories.”

This concurs the Ayurvedic idea of Panchkoshiya sharir where above physical body, Prana and Mind play essential role in forming memories and taking actions.


Research


Reinstatement of long-term memory following erasure of its behavioral and synaptic expression in Aplysia

Long-term memory (LTM) is believed to be stored in the brain as changes in synaptic connections. Here, we show that LTM storage and synaptic change can be dissociated. Cocultures of Aplysia sensory and motor neurons were trained with spaced pulses of serotonin, which induces long-term facilitation. Serotonin (5HT) triggered growth of new presynaptic varicosities, a synaptic mechanism of long-term sensitization. Following 5HT training, two antimnemonic treatments—reconsolidation blockade and inhibition of PKM—caused the number of presynaptic varicosities to revert to the original, pretraining value. Surprisingly, the final synaptic structure was not achieved by targeted retraction of the 5HT-induced varicosities but, rather, by an apparently arbitrary retraction of both 5HT-induced and original synapses. In addition, we find evidence that the LTM for sensitization persists covertly after its apparent elimination by the same antimnemonic treatments that erase learning-related synaptic growth. These results challenge the idea that stable synapses store long-term memories.

DOI: http://dx.doi.org/10.7554/eLife.03896.001

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