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Jan 28, 2017 – Donald Trump during the presidential campaign. … Of these three players—reflectiveKosinski, carefully groomed Nix and grinning … accuracy), and their affiliation to the Democratic or Republican party (85 percent). …. chief executive officer of Cambridge Analytica,” a smooth female voice announces.
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Source: Duke University.
Brains are made of more than a tangled net of neurons. Star-like cells called astrocytes diligently fill in the gaps between neural nets, each wrapping itself around thousands of neuronal connections called synapses. This arrangement gives each individual astrocyte an intricate, sponge-like structure.
New research from Duke University finds that astrocytes are much more than neurons’ entourage. Their unique architecture is also extremely important for regulating the development and function of synapses in the brain.
When they don’t work right, astrocyte dysfunction may underlie neuronal problems observed in devastating diseases like autism, schizophrenia and epilepsy.
The Duke team identified a family of three proteins that control the web-like structure of each astrocyte as it grows and encases neuronal structures such as synapses. Switching off one of these proteins not only limited the complexity of the astrocytes, but also altered the nature of the synapses between neurons they touched, shifting the delicate balance between excitatory and inhibitory neural connections.
“We found that astrocytes’ shape and their interactions with synapses are fundamentally important for brain function and can be linked to diseases in a way that people have neglected until now,” said Cagla Eroglu, an associate professor of cell biology and neurobiology at Duke. The research was published in the Nov. 9 issue of Nature.
Astrocytes have been around almost as long as brains have. Even simple invertebrates like the crumb-sized roundworm C. elegans has primitive forms of astrocytes cloaking their neural synapses. As our brains have evolved into complex computational machines, astrocyte structure has also grown more elaborate.
But the complexity of astrocytes is dependent on their neuronal companions. Grow astrocytes and neurons together in a dish, and the astrocytes will form intricate star-shaped structures. Grow them alone, or with other types of cells, and they come out stunted.
To find out how neurons influence astrocyte shape, Jeff Stogsdill, a recent PhD graduate in Eroglu’s lab, grew the two cells together while tweaking neurons’ cellular signaling mechanisms. He was surprised to find that even if he outright killed the neurons, but preserved their structure as a scaffold, the astrocytes still beautifully elaborated on them.
“It didn’t matter if the neurons were dead or alive — either way, contact between astrocytes and neurons allowed the astrocyte to become complex,” Stogsdill said. “That told us that there are interactions between the cell surfaces that are regulating the process.”
Stogsdill searched existing genetic databases for cell surface proteins known to be expressed by astrocytes, and identified three candidates that might help direct their shape.
Previously, their functions had been primarily studied in neurons.
To find out what role neuroligins play in astrocytes, Stogsdill tinkered with astrocytes’ ability to produce these proteins. He found that when he switched off the production of neuroligins, the astrocytes grew small and blunt. But when he boosted the production of neuroligins, astrocytes grew to nearly twice the size.
“The shape of the astrocytes was directly proportional to their expression of the neuroligins,” Stogsdill said.
Tweaking the expression of neuroligins didn’t just change the size and shape of the astrocytes. They also had a drastic effect on the synapses that astrocyte touched.
When Stogsdill switched off a single neuroligin — neuroligin 2 — the number of excitatory or “go” synapses dropped by 50 percent. The number of inhibitory or “stop” synapses stayed the same, but their activity increased.
Stogsdill said. “Which just drives home that these disease-associated molecules are potentially functioning in astrocytes to shift this balance.”
Ben Barres, a professor of neurobiology at Stanford University who was not involved with the study, praised the findings as “a profoundly important, revolutionary advance” for understanding how interactions between neurons and astrocytes can affect synapse formation.
“To ignore the astrocytes, which are vastly more numerous than neurons, is always a mistake.”
Other authors on the study are Juan Ramirez, Katherine T. Baldwin, Eray Enustun, Tiffany Ejikeme from Duke University Cell Biology Department and Ru-Rong Ji, Di Liu, Yong-Ho Kim from Duke University Department of Anesthesiology.
Funding: This research was supported by grants from the National Institutes of Health (RO1 DA031833, RO1 DE022743 and F31 NS092419) and a Holland Trice Brain Research Award. Additional support was provided by the Foerster-Bernstein Family and the Hartwell Foundation.
Source: Kara Manke – Duke University
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited toJeff Stogsdill, Duke University.
Original Research: Abstract for “Astrocytic neuroligins control astrocyte morphogenesis and synaptogenesis” by Jeff A. Stogsdill, Juan Ramirez, Di Liu, Yong-Ho Kim, Katherine T. Baldwin, Eray Enustun, Tiffany Ejikeme, Ru-Rong Ji and Cagla Eroglu in Nature. Published online November 8 2017 doi:10.1038/nature24638
Full open access research for “Cell Biology of Astrocyte-Synapse Interactions” by Nicola J. Allen and Cagla Eroglu in Neuron. Published online November 1 2017 doi:10.1016/j.neuron.2017.09.056
Abstract
Astrocytic neuroligins control astrocyte morphogenesis and synaptogenesis
Astrocytes are complex glial cells with numerous fine cellular processes that infiltrate the neuropil and interact with synapses. The mechanisms that control the establishment of astrocyte morphology are unknown, and it is unclear whether impairing astrocytic infiltration of the neuropil alters synaptic connectivity. Here we show that astrocyte morphogenesis in the mouse cortex depends on direct contact with neuronal processes and occurs in parallel with the growth and activity of synaptic circuits.
Our findings highlight a previously undescribed mechanism of action for neuroligins and link astrocyte morphogenesis to synaptogenesis.
“Astrocytic neuroligins control astrocyte morphogenesis and synaptogenesis” by Jeff A. Stogsdill, Juan Ramirez, Di Liu, Yong-Ho Kim, Katherine T. Baldwin, Eray Enustun, Tiffany Ejikeme, Ru-Rong Ji and Cagla Eroglu in Nature. Published online November 8 2017 doi:10.1038/nature24638
Abstract
Cell Biology of Astrocyte-Synapse Interactions
Astrocytes, the most abundant glial cells in the mammalian brain, are critical regulators of brain development and physiology through dynamic and often bidirectional interactions with neuronal synapses. Despite the clear importance of astrocytes for the establishment and maintenance of proper synaptic connectivity, our understanding of their role in brain function is still in its infancy. We propose that this is at least in part due to large gaps in our knowledge of the cell biology of astrocytes and the mechanisms they use to interact with synapses.
Furthermore, we pose some pressing questions that need to be addressed to advance our mechanistic understanding of the role of astrocytes in regulating synaptic development.
“Cell Biology of Astrocyte-Synapse Interactions” by Nicola J. Allen and Cagla Eroglu in Neuron. Published online November 1 2017 doi:10.1016/j.neuron.2017.09.056
Source: DGIST.
DGIST’s research team led by Dr. Yun-Il Lee in Well Aging Research Center has identified a new mechanism of inhibition of dopaminergic neuronal apoptosis and suggested the possibility of preventing and treating Parkinson’s disease.
Parkinson’s disease (PD) is a typical degenerative brain disease caused by the death of dopaminergic neurons in the middle cerebral blood. It is a disease with a higher incidence in the population aged 60 or older, exhibiting symptoms such as tremor, stiffness, slow motion and postural instability.
In particular, as the majority of Parkinson’s patients suffer from the progressive neurodegenerative disease, many researchers newly started to focus on cell death, a loss of dopamine-producing neurons, to treat PD. With regard to the cell death process, in vivo cell stress and damages activate PARP-1 (Poly ADP-ribose polymerase-1) and induce excessive accumulation of PAR (Poly ADP-ribose) and those activities activate AIF (Apoptosis-Inducing Factor), a factor that induces cell death, and destroy DNA. This new mechanism of cell death (Parthanatos) has recently been known as the cause of degenerative brain diseases such as Parkinson’s disease, stroke, heart attack, diabetes, etc. and the mechanism has been extensively studied as previous research to treat these diseases.
Currently, medications are being used to alleviate symptoms of Parkinson’s disease. However, there are no government-approved drugs that can inhibit dopaminergic neuronal cell death. Then, the research teams have found the possibility in licorice, the herb medicine.
Dr. Yun-Il Lee carried out joint research with Professor Joo-Ho Shin and Professor Yunjong Lee from Sungkyunkwan University School of Medicine to study candidate compounds for the treatment of Parkinson’s disease. For example, the researchers have identified the mechanism that cortisol, a stress hormone, promotes dopaminergic neuronal activity by inducing parkin protein expression that inhibits dopamine neuronal cell death.
In this study, the research teams found the candidate drugs that induce the expression of RNF146 protein involved in the inhibition of neuronal cell death through high-speed mass screening method using the natural materials library of the Natural Medicine Bank of Korea Foundation.
As a result, the study has confirmed that liquiritigenin, a licorice extract, induces the expression of RNF146 protein and removes excessively accumulated PAR binding and modified substrate proteins using the ubiquitin proteasome system and results in inhibition of dopamine neuronal cell death.
In addition, the research teams have been working on identifying the mechanism which induces liquiritigenin’s RNF146 protein expression and demonstrated that it regulates transcription through binding and activity with estrogen receptors in cell and animal models. Consequently, it has been scientifically proved that liquiritigenin, a licorice extract, can be used as a treatment for degenerative Parkinson’s disease.
Dr. Yun-Il Lee stated “Neuronal death is involved in a variety of signaling systems in vivo. Therefore, it is essential to identify a new mechanism that is able to control the system comprehensively and we have found additional possibilities in licorice extract.” He added “I would like to contribute to the treatment of degenerative brain diseases such as Parkinson’s disease by conducting advanced researches, comprehensive research and clinical studies.”
Source: Dajung Kim – DGIST
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited to Daegu Gyeongbuk Institute of Science and Technology (DGIST).
Original Research: Full open access research for “Estrogen receptor activation contributes to RNF146 expression and neuroprotection in Parkinson’s disease models” by Hyojung Kim, Sangwoo Ham, Joon Yeop Lee, Areum Jo, Gum Hwa Lee, Yun-Song Lee, MyoungLae Cho, Heung-Mook Shin, Donghoon Kim, Olga Pletnikova, Juan C. Troncoso, Joo-Ho Shin, Yun-Il Lee and Yunjong Lee in Oncotarget. Published online November 2017 doi:10.18632/oncotarget.21828
Abstract
Estrogen receptor activation contributes to RNF146 expression and neuroprotection in Parkinson’s disease models
RNF146 is an E3 ubiquitin ligase that specifically recognizes and polyubiquitinates poly (ADP-ribose) (PAR)-conjugated substrates for proteasomal degradation. RNF146 has been shown to be neuroprotective against PAR polymerase-1 (PARP1)-induced cell death during stroke. Here we report that RNF146 expression and RNF146 inducers can prevent cell death elicited by Parkinson’s disease (PD)-associated and PARP1-activating stimuli. In SH-SY5Y cells, RNF146 expression conferred resistance to toxic stimuli that lead to PARP1 activation. High-throughput screen using a luciferase construct harboring the RNF146 promoter identified liquiritigenin as an RNF146 inducer. We found that RNF146 expression by liquiritigenin was mediated by estrogen receptor activation and contributed to cytoprotective effect of liquiritigenin. Finally, RNF146 expression by liquiritigenin in mouse brains provided dopaminergic neuroprotection in a 6-hydroxydopamine PD mouse model. Given the presence of PARP1 activity and RNF146 deficits in PD, it could be a potential therapeutic strategy to restore RNF146 expression by natural compounds or estrogen receptor activation.
“Estrogen receptor activation contributes to RNF146 expression and neuroprotection in Parkinson’s disease models” by Hyojung Kim, Sangwoo Ham, Joon Yeop Lee, Areum Jo, Gum Hwa Lee, Yun-Song Lee, MyoungLae Cho, Heung-Mook Shin, Donghoon Kim, Olga Pletnikova, Juan C. Troncoso, Joo-Ho Shin, Yun-Il Lee and Yunjong Lee in Oncotarget. Published online November 2017 doi:10.18632/oncotarget.21828
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A new study shows for the first time that gut bacteria from old mice induce age-related chronic inflammation when transplanted into young mice. Called “inflammaging,” this low-grade chronic inflammation is linked to life-limiting conditions such as stroke, dementia and cardiovasuclar disease. The research, published today in open-access journal Frontiers in Immunology, brings the hope of a potentially simple strategy to contribute to healthy ageing, as the composition of bacteria in the gut is, at least in part, controlled by diet.
“Since inflammaging is thought to contribute to many diseases associated with ageing, and we now find that the gut microbiota plays a role in this process, strategies that alter the gut microbiota composition in the elderly could reduce inflammaging and promote healthy ageing,” explains Dr Floris Fransen, who performed the research at the University Medical Center Groningen, The Netherlands. “Strategies that are known to alter gut microbiota composition include changes in diet, probiotics, and prebiotics.”
Previous research shows that the elderly tend to have a different composition of gut bacteria than younger people.
Knowing this, Fransen and his team set out to investigate a potential link.
The scientists transferred gut microbiota from old and young conventional mice to young germ-free mice, and analysed immune responses in their spleen, lymph nodes and tissues in the small intestine. They also analysed whole-genome gene expression in the small intestine.
The results suggest that an imbalance of the bacterial composition in the gut may be the cause of inflammaging in the elderly. Imbalances, or “dysbiosis” of gut bacteria results in “bad” bacteria being more dominant than “good” bacteria. An overgrowth of bad bacteria can make the lining of the gut become more permeable, allowing toxins to enter the bloodstream where they can travel around the body with various negative effects.
“Our gut is inhabited by a huge number of bacteria” explains Fransen. “Moreover, there are many different kinds of bacterial species, and the bacterial species that are present can vary a lot from person to person.”
Maintaining a healthy gut microbiota is clearly important to a healthy body and healthy ageing, but why the gut microbiota is different in the elderly is not fully understood. Many people are aware of the effect a course of antibiotics can have on the digestive system for example, but as Fransen explains, it may not be down to just one thing: “It is likely a combination of factors such as reduced physical activity, changes in diet, but also as part of a natural process.”
Most, if not all, age-related diseases can be linked back to inflammaging. Despite the fact that this particular study was conducted on mice, it is clear that maintaining a healthy gut microbiota is key to a healthy lifestyle. However, more research is needed to confirm that the human body mirrors the mice in this study.
“Both in humans and mice there is a correlation between altered gut microbiota composition and inflammaging, but the link between the two remains to be proven in humans” concludes Fransen.
The article is part of the Frontiers Research Topic Immunomodulatory Functions of Nutritional Ingredients in Health and Disease.
Source: Frontiers
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Full open access research for “Aged Gut Microbiota Contributes to Systemical Inflammaging after Transfer to Germ-Free Mice” by Floris Fransen, Adriaan A. van Beek, Theo Borghuis, Sahar El Aidy, Floor Hugenholtz, Christa van der Gaast – de Jongh, Huub F. J. Savelkoul, Marien I. De Jonge, Mark V. Boekschoten, Hauke Smidt, Marijke M. Faas, and Paul de Vos in Frontiers in Immunology. Published online November 2 2017 doi:10.3389/fimmu.2017.01385
Abstract
Aged Gut Microbiota Contributes to Systemical Inflammaging after Transfer to Germ-Free Mice
Advanced age is associated with chronic low-grade inflammation, which is usually referred to as inflammaging. Elderly are also known to have an altered gut microbiota composition. However, whether inflammaging is a cause or consequence of an altered gut microbiota composition is not clear. In this study, gut microbiota from young or old conventional mice was transferred to young germ-free (GF) mice. Four weeks after gut microbiota transfer immune cell populations in spleen, Peyer’s patches, and mesenteric lymph nodes from conventionalized GF mice were analyzed by flow cytometry. In addition, whole-genome gene expression in the ileum was analyzed by microarray. Gut microbiota composition of donor and recipient mice was analyzed with 16S rDNA sequencing. Here, we show by transferring aged microbiota to young GF mice that certain bacterial species within the aged microbiota promote inflammaging. This effect was associated with lower levels of Akkermansia and higher levels of TM7 bacteria and Proteobacteria in the aged microbiota after transfer. The aged microbiota promoted inflammation in the small intestine in the GF mice and enhanced leakage of inflammatory bacterial components into the circulation was observed. Moreover, the aged microbiota promoted increased T cell activation in the systemic compartment. In conclusion, these data indicate that the gut microbiota from old mice contributes to inflammaging after transfer to young GF mice.
“Aged Gut Microbiota Contributes to Systemical Inflammaging after Transfer to Germ-Free Mice” by Floris Fransen, Adriaan A. van Beek, Theo Borghuis, Sahar El Aidy, Floor Hugenholtz, Christa van der Gaast – de Jongh, Huub F. J. Savelkoul, Marien I. De Jonge, Mark V. Boekschoten, Hauke Smidt, Marijke M. Faas, and Paul de Vos in Frontiers in Immunology. Published online November 2 2017 doi:10.3389/fimmu.2017.01385
What does this mean? When we are busy focusing or doing some focused task, we cannot feel some other sensation including pain. So I experimented on childbirth pain issue by focusing on the baby coming out of the birth canal and when my focus is off, I can feel more pain.
Connie
Bursts of Beta Waves, Not Sustained Rhythms, Filter Sensory Processing in Brain
Summary: In both human and animal subject, bursts of beta wave activity in the brain help to filter distraction in order to process different sensations, a new study reports.
Source: Brown University.
To better understand the brain and to develop potential therapies, neuroscientists have been investigating how “beta” frequency brainwaves help the brain filter distractions to process sensations. A new Brown University study stands to substantially refine what they thought was going on: What really matters is not a sustained elevation in beta wave power, but instead the rate of specific bursts of beta wave activity, ideally with perfect timing.
The new insight, reported in the journal eLife, arose from the scientists looking beneath the covers of the typical practice of averaging beta brain wave data. With a closer examination, trial-by-trial for each subject, they saw that what really reflected attention and impacted perception were discrete, powerful bursts of beta waves at frequencies around 20 hertz.
“When people were trying to block distraction in a brain area, the probability of seeing these beta events went up,” said senior author Stephanie R. Jones, an associate professor of neuroscience at Brown. “The brain seemed to be flexibly modulating the expression of these beta events for optimal perception.”
The findings, made with consistency in humans and mice, can not only refine ongoing research into how beta waves arise and work in the brain, Jones said, but also provide guidance to clinicians as they develop therapies that seek to modulate beta waves.
Testing touch
The research team, led by graduate student Hyeyoung Shin, acquired the data through a series of experiments in which they measured beta waves in the somatosensory neocortex of humans and mice in the second leading up to inducing (or not inducing) varying amounts of a tactile sensation. Humans wore a cap of magnetoencephalography sensors, while mice had implanted electrodes. For people, the sensation was a tap on a finger tip or the foot. For mice, it was a wiggle of a whisker.
Subjects were merely required to report the sensations they felt — people pushed a button, while mice were trained to lick a sensor in exchange for a reward. The researchers tracked the association of beta power with whether subjects accurately detected, or didn’t detect, stimuli. What they found, as expected, is that the more beta activity there was in the corresponding region of cortex, the less likely subjects were to report feeling a sensation. Elevated beta activity is known to help suppress distractions.
A particularly good example, Shin said, was that in experiments where people were first instructed to focus on their foot, there was more beta power in the hand region of the neocortex. Correspondingly, more beta in the hand region resulted in less detection of a sensation in the hand.
“We think that beta acts a filter mechanism,” Shin said.
Beta bursts
Consistently throughout various iterations of the experiments across both the human and mouse subjects, increases in beta activity did not manifest as a continuously elevated rhythm. Instead, when beta appeared, it quickly spiked in short, distinct bursts of power. Only if a subject’s beta was averaged over many trials would it look like a smooth plateau of high-power activity.
After discovering this pattern, the researchers performed analyses to determine what features of the bursts best predicted whether subjects would report, or miss, a touch sensation. After all, it could be the number of bursts, their power, or maybe how long they lasted.
What Shin and the team found is that number of bursts and their timing both mattered independently. If there were two or more bursts any time in the second before a sensation, it was significantly more likely to go undetected. Alternatively, if just one burst hit within 200 milliseconds of the sensation, the stimulus would also be more likely to be overlooked.
“The ideal case was having large numbers and being close in timing to the stimulus,” Shin said.
A better idea of beta
While the study helps to characterize the nature of beta in the somatosensory neocortex, it doesn’t explain how it affects sensations, Jones acknowledged. But that’s why it is important that the results were in lockstep in both mice and in people. Confirming that mice model the human experience means researchers can rely on mice in experiments that delve more deeply into how beta bursts arise and what their consequence are in neurons and circuits. Shin is already doing experiments to dissect how distinct neural subpopulations contribute to beta bursts and somatosensory detection, respectively. Co-author and postdoctoral researcher Robert Law is applying computational neural models that link the human and animal recordings for further discovery.
In the clinical realm, Jones said, an improved understanding of how beta works could translate directly into improving therapies such as transcranial magnetic stimulation or transcranial alternating current to treat neurological disorders, such as chronic pain, or depression. Rather than using those technologies to generate a consistent elevation in beta in a brain region, Jones said, it might be more effective to use them to induce (or suppress) shorter, more powerful bursts and to time those to be as close in time to a target brain activity as possible.
“Typically with non-invasive brain stimulation you are trying to entrain a rhythm,” Jones said. “What our results suggest is that’s not what the brain is doing. The brain is doing this intermittent pattern of activity.”
The findings could also help scientists better understand other beta-associated disorders, such as Parkinson’s disease or obsessive compulsive disorder, and influence brain computer interfaces that rely on beta activity.
The paper’s other authors are Shawn Tsutsui and Christopher Moore.
Funding for the research came from the National Institutes of Health, the U.S. Department of Veterans Affairs, the National Science Foundation, the Brown Institute for Brain Science and the Fulbright Association.
Source: David Orenstein – Brown University
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited to Shin et. al./Brown University.
Original Research:Abstract for “The rate of transient beta frequency events predicts behavior across tasks and species” by Hyeyoung Shin, Robert Law, Shawn Tsutsui, Christopher I Moore, and Stephanie R Jones in eLife. Published online November 6 2017 doi:10.7554/eLife.29086
Abstract
The rate of transient beta frequency events predicts behavior across tasks and species
Beta oscillations (15-29Hz) are among the most prominent signatures of brain activity. Beta power is predictive of healthy and abnormal behaviors, including perception, attention and motor action. In non-averaged signals, beta can emerge as transient high-power ‘events’. As such, functionally relevant differences in averaged power across time and trials can reflect changes in event number, power, duration, and / or frequency span. We show that functionally relevant differences in averaged beta power in primary somatosensory neocortex reflect a difference in the number of high-power beta events per trial, i.e. event rate.
Further, beta events occurring close to the stimulus were more likely to impair perception. These results are consistent across detection and attention tasks in human magnetoencephalography, and in local field potentials from mice performing a detection task. These results imply that an increased propensity of beta events predicts the failure to effectively transmit information through specific neocortical representations.
“The rate of transient beta frequency events predicts behavior across tasks and species” by Hyeyoung Shin, Robert Law, Shawn Tsutsui, Christopher I Moore, and Stephanie R Jones in eLife. Published online November 6 2017 doi:10.7554/eLife.29086
Bursts of beta activity are associated with a strengthening of sensory feedback in static motor control and reduced when there is movement change.
The artificial induction of increased beta waves over the motor cortex by a form of electrical stimulation called Transcranial alternating-current stimulation consistent with its link to isotonic contraction produces a slowing of motor movements.
Diffuse beta waves present alongside other frequencies in spontaneous EEG recorded from a 28-month-old child with Dup15q syndrome.
Beta waves are often considered indicative of inhibitory cortical transmission mediated by gamma aminobutyric acid (GABA), the principal inhibitory neurotransmitter of the mammalian nervous system. Benzodiazepines, drugs that modulate GABAA receptors, induce beta waves in EEG recordings from humans [8] and rats.[9] Spontaneous beta waves are also observed diffusely in scalp EEG recordings from children with duplication 15q11.2-q13.1 syndrome (Dup15q) who have duplications of GABAA receptor subunit genes GABRA5, GABRB3, and GABRG3.[10] For this reason, it is possible that, in certain clinical contexts, beta waves could be a general biomarker of GABAA receptor gene overexpression or otherwise aberrant GABAergic transmission.
Rangaswamy M, Porjesz B, Chorlian DB, Wang K, Jones KA, Bauer LO, Rohrbaugh J, O’Connor SJ, Kuperman S, Reich T, Begleiter (2002). “Beta power in the EEG of alcoholics”. BIOLOGICAL PSYCHOLOGY. 52 (8): 831–842. doi:10.1016/s0006-3223(02)01362-8. PMID 12372655.
Jump up ^ Buzsáki, György (2006). Rhythms of the Brain. New York: Oxford University Press. p. 4.
Jump up ^ Baumeister J, Barthel T, Geiss KR, Weiss M (2008). “Influence of phosphatidylserine on cognitive performance and cortical activity after induced stress”. NUTRITIONAL NEUROSCIENCE. 11 (3): 103–110. doi:10.1179/147683008X301478. PMID 18616866.
Jump up ^ Baker, SN (2007). “Oscillatory interactions between sensorimotor cortex and the periphery”. Current Opinion in Neurobiology. 17 (6): 649–55. doi:10.1016/j.conb.2008.01.007. PMC 2428102 Freely accessible. PMID 18339546.
Jump up ^ Lalo, E; Gilbertson, T; Doyle, L; Di Lazzaro, V; Cioni, B; Brown, P (2007). “Phasic increases in cortical beta activity are associated with alterations in sensory processing in the human”. Experimental brain research. Experimentelle Hirnforschung. Experimentation cerebrale. 177 (1): 137–45. doi:10.1007/s00221-006-0655-8. PMID 16972074.
Jump up ^ Zhang, Y; Chen, Y; Bressler, SL; Ding, M (2008). “Response preparation and inhibition: the role of the cortical sensorimotor beta rhythm”. Neuroscience. 156 (1): 238–46. doi:10.1016/j.neuroscience.2008.06.061. PMC 2684699 Freely accessible. PMID 18674598.
Jump up ^ Pogosyan, A; Gaynor, LD; Eusebio, A; Brown, P (2009). “Boosting cortical activity at Beta-band frequencies slows movement in humans”. Current Biology. 19 (19): 1637–41. doi:10.1016/j.cub.2009.07.074. PMC 2791174 Freely accessible. PMID 19800236.
Jump up ^ Feshchenko, V; Veselis, R; Reinsel, R (1997). “Comparison of the EEG effects of midazolam, thiopental, and propofol: the role of underlying oscillatory systems”. Neuropsychobiology. PMID 9246224.
Jump up ^ Van Lier, Hester; Drinkenburg, Wilhelmus; Van Eeten, Yvonne; Coenen, Anton (2004). “Effects of diazepam and zolpidem on EEG beta frequencies are behavior-specific in rats”. Neuropharmacology. Retrieved 4 January 2017.
Jump up ^ Frohlich, Joel; Senturk, Damla; Saravanapandian, Vidya; Golshani, Peyman; Reiter, Lawrence; Sankar, Raman; Thibert, Ronald; DiStefano, Charlotte; Huberty, Scott; Cook, Edwin; Jeste, Shafali (December 2016). “A Quantitative Electrophysiological Biomarker of Duplication 15q11.2-q13.1 Syndrome” (PDF). PLOS One. Retrieved 4 January 2017.
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| Eggplant and apple cider vinegar for skin cancer | |
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| Philippines Coconut Wine -Tuba | |
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| What the Paradise papers reveal about Trump’s inner circle, Russian connections | |
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| When will Souvenaid become available in Canada and US to treat Alzheimer’s Disease? | |
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| MEDICATIONS TO AVOID that worse PD (Parkinson’s disease) | |
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| Sleep to lower your blood glucose level in the brain | |
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| Cost of staying young and delaying aging | |
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| Top aging hacks 11-7-2017 | |
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| Increase the body’s oxygen carrying capacity with exercise, EPO and whole foods | |
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| Complications of Low Potassium and sodium and magnesium for balance | |
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| Non pasteurized beers have more health benefits | |
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| Can Gout be cured permanently? | |
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| Oxidative Stress, Inflammation, Thyroid and Anti-oxidant | |
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| Aging hacks Nov 2017 | |
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| Growth hormone DHEA increases libido/anti-aging | |
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| Detox your lungs from air pollution and metal toxins and for early lung cancer | |
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| Skin and nerves need Vit C, A, D, E, calcium-magnesium and B complex | |
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| Fight VIRUS with Enzymes from pineapple and papaya, baking soda, alkaline food, calcium and magnesium from whole foods | |
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| Signs of the preactive/ active phase of dying and medications for terminally ill | |
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| Cash flow analysis worksheet template | |
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| V02 – Older persons must keep training like endurance athlete to ward off age decline | |
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| From healthy to 7 list of health issues which started by hitting toe on door | |
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| Foods to eat and avoid when you have Gout and leg pains | |
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| Brain activity ripples linked to creation of long-term memories – sleep more | |
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| Excessive sweating and Parkinsons | |
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| Vitamins to take while working out | |
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| Can high SGPT and SGOT lead to heart disease? | |
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| Old Human Cells Rejuvenated – resveratrol in dark choco, berries and grapes | |
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| Aging and resveratrol in berries and grapes | |
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| Avoid chronic bronchitis with green apple, onions, garlic, vinegar and rest | |
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| Donate blood to help your body and other people | |
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| Parkinson and Exercises | |
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| Trends in medical health insurance, costs and expenses by state | |
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| Jan 27-28 2018 National Drug and Alcohol facts week | |
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| Cost of staying young | |
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| Lung cancer in the Philippines | |
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| Depression and PTSD are health problems faced by our VETs | |
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| How diet can change your epigenome and affect cancer and chromatin of DNA | |
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| Top aging hacks 11-6-2017 | |
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| Demand an independent investigation into Trump’s ties to Russia | |
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| Restless Legs Syndrome in Alzheimer’s and Parkinson’s Disease | |
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| Study reveals role of specific lipids in accelerating or curbing bacterial infection | |
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| Urgent need for gun safety laws | |
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| Healthy Gut Healthy Brain by Dr David Perlmutter | |
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| Universal health care would save us $17 trillion | |
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| Does drinking warm water reduce cholesterol? | |
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| Hiatal Hernia, Pancreatitis, Pancreatic Cancer and the Western Diet | |
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| How can we increase the hemoglobin content in our blood? | |
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| Our condolence to the family of Anniek Henk | |
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| Psoriasis, immune system and nutrition | |
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| Good fats, SCFA – short chain fatty acids | |
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| 16 Tips On How To Treat HPV Naturally And Effectively At Home | |
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| Yohimbine and sleep apnea | |
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| Acetylcholine/Choline Deficiency in Chronic Illness – mental, liver, kidney, heart and hormones | |
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| Protect your eyes and kidneys with anti-oxidants | |
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| Browning or caramelized sugar is a carcinogen | |
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| Combat the Silent Dangers of High Uric Acid naturally | |
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| Degenerative Joint Disease by Dr Axe | |
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| Root cause analysis in health care | |
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| Mike Pence Implicated in Treason Scandal | |
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| Will Sessions throw Trump under the bus to save himself? | |
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| Neck pain and MTHFR gene , folate , methionine | |
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| Toddlers constipated from whole milk, what to do | |
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| Fenugreek, for diabetes/lactating moms/to boost testosterone | |
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| Iodine prevents cancer growth; up avocado and reduce caffeine intake to prevent Thyroid cancer | |
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| Reducing belly fat | |
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| Eat protein-rich food when drinking alcohol to protect your stomach | |
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| Hair Loss/Weight Loss, herbs for allergies, drug side-effects, herbs with caution, chemo Q&A | |
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| Samsung and WellDoc partner to offer direct-to-consumer version of diabetes management app | |
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| Nitric Oxide for strong blood vessels’ cells , up with exercise, melons, cucumber, Vit C, E, amino acid – L-arginine, L-citrulline | |
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| Glutathione, the body’s master antioxidant and detoxifier by Priya Shah | |
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| 12 Life Lessons along the Path to Enlightenment by David R. Hawkins, M.D. Ph.D. | |
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| 1 | |
| Mullein herb for lung and breast health – COPD signs, symptoms and diagnosis | |
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| 100 WTF Moments From Trump’s First 100 Days | |
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| 1 | |
| Own Worldgn stock, earn more and get your fitness tracker to monitor health | |
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| Health issues in developing and industrialized countries | |
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| Folate – Vit B9 deficiency or MTHFR gene mutation | |
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| Business ownership, real estate and paper assets are your path to wealth building | |
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| Should I take my mom with Alzheimer’s to Peru to see a curandero? | |
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| Ionizing radiation may be confounding factor in Alzheimer’s disease | |
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| Anti-aging Vitamin B3, Niacin | |
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| Vitamin D Promotes Protein Homeostasis and Longevity via the Stress Response Pathway Genes | |
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| To spread, nervous system viruses – herpes – sabotage cell, hijack transportation | |
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| Religious Beliefs Activate Neural Reward Circuits in Same Way As Sex and Drugs | |
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| Folate – Vit B9 deficiency or MTHFR gene mutation | |
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| How important is the thymus gland in keeping your body free from diseases? | |
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| Fitness tracker, pain relief and home health monitor with HELO smart band | |
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| No grains, dairy, processed foods and sugars for active Crohn’s disease and ulcerative colitis | |
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| Glia, Not Neurons, Most Affected By Brain Aging | |
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| Monitor important vitals at home with a wearable not just exercise level | |
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| What is Precision, predictive and Personalize Medicine vs patient-centered care | |
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| 1 | |
| Tell TV networks: Stop broadcasting Trump’s lies | |
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| 1 | |
| Paul Ryan and Mitch McConnell implicated in Russia-Trump | |
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| 1 | |
| Find a town hall rally near you – health care is human right | |
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| Can balsamic vinegar help with gout? | |
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| Anti-aging and Parkinson/Alzheimer’s prevention: Enzymes and apple cider vinegar | |
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| Top aging hacks 11-3-2017 | |
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| Gastroparesis, Betain HCL, diabetes and stomach health | |
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| Shatter Me Featuring Lzzy Hale – Lindsey Stirling | |
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| Nitric Oxide Dump Exercise with nose breathing to lower blood pressure and thin blood | |
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| Paul Ryan and Mitch McConnell implicated in Russia-Trump | |
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| Anti-aging and repairs DNA – Niacin in Avocado, peanuts and turkey | |
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| Robert Reich: The Resistance Report 10-30-2017 | |
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| News Medical Life Sciences | |
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| Sarah Huckabee Sanders | |
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| Protect your eyes and kidneys with anti-oxidants | |
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| Homeless camps contrast with West Coast tech wealth | |
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| Slow the aging process by lengthening your telomeres | |
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| Inflammation , brain and your health | |
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| Zinc jams shut a protein transporter in bacteria preventing infection this winter | |
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| Washington Post: Opinion section | |
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| Trump’s Clueless Abdication of Presidential Responsibility | |
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| 1 | |
| Universal health care would save us $17 trillion | |
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| Top posts 7-31-2017 | |
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| Voter suppression: how much Trump’s commission is spending to investigate fake voter fraud allegations | |
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| Harvard Health Letter | |
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| Unfit to serve T-shirts | |
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| Recovering from stroke with proper nutrition | |
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| Psoriasis, immune system and nutrition | |
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| Nettle leaf tea and cranberries cured her UTI | |
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| Prison costs in the USA | |
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| A balance of dopamine and serotonin for your brain function | |
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| Fatigue and Red (bloodshot) eyes from WebMD | |
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| Vitamin B and Pineapple for nerve damage by Dr E. Kane | |
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| Traumatic brain injury, lack of sleep, aging = Alzheimer/Dementia | |
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| Atopic dermatitis and psoriasis by Dr Mercola | |
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| Guava and water apple to fight diabetes | |
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| Philippines president Dutarte asked each town to prepare a list of drug users and pushers | |
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| What’s a good analogy to explain the immune system? | |
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| Anabolic and catabolic process, hormones and exercise | |
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| Magic Mushrooms May ‘Reset’ Brains of Depressed Patients | |
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| Eye inflammation and gut bacteria | |
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| Toxicology test for pregnant women | |
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| Growth hormone in male infertility | |
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| How does a CBC test for a leukemia patient usually look like? | |
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| Eggplant and apple cider vinegar for skin cancer | |
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| How to know if your supplements are working for you? | |
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| Our condolence to the family of Anniek Henk | |
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| Inflammation to colitis to Alzheimer’s disease | |
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| One Virus and Two Types of Bacteria as Major Causes of Alzheimer’s |
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