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Category: neuroscience – Page 801

Digital Presentism: D-Theory of Time

#DigitalPresentism #DTheoryofTime #TemporalMechanics

Temporal philosophy is a fascinating but eerily difficult topic. Correctly answering the philosophical questions and paradoxes of time paves the way to unlocking one of the last remaining mysteries of mind since our perception of time and consciousness, as you know, are simply inseparable. A new theory of time, Digital Presentism, comes from the triangulation of temporal physics, digital physics and experiential realism. This essay addresses the flaming questions in philosophy of time: “Is time fundamental or emergent?”, “How does time exist, if at all?”, “How can we update the current epistemic status of temporal ontology?” For starters, let’s recap what we’ve learned so far about physics of time. Here’s a quick summary: in Time Series essays, we dissected the nature of time through the prism of these 7 common misconceptions:

Holo Syntellectus: Are We Evolving into a New Cybernetic Species Interlinked into the Global Mind?

Behind all this doom and gloom, the current COVID-19 viral threat, dreaded climate disasters and feared robocalypse, it’s hard to see a bigger and amazingly brighter picture. Are we evolving into a new species with hybrid thinking, interlinked into the Global Mind? Once our neocortices are seamlessly connected to the Web, what will that feel like to step up one level above human consciousness to global consciousness? Any crisis, including the current one, is an opportunity to transcend the quagmire of status quo.

Are we evolving into a new species with hybrid thinking, interlinked into the Global Mind? At what point may the Web become self-aware? Once our neocortices are seamlessly connected to the Web, how will that feel like to step up one level above human consciousness to global consciousness?

In his book “The Global Brain” (2000) Howard Bloom argues that hyperconnected humans and machines resemble a lot the neurons of the “global brain,” and the coming Internet of Things (IoT) with trillions of sensors around the planet will become effectively the nervous system of Earth. According to the Gaia hypothesis by James Lovelock, we have always been an integral part of this “Meta-Mind,” collective consciousness, global adaptive and self-regulating system while tapping into vast resources of information pooling and at the same time having a “shared hallucination,” we call reality.

The Difference Between Success and Failure: (Neuro)science of Getting and Staying Motivated

There is no question that motivation is one of the hardest and yet important factors in life. It’s the difference between success and failure, goal-setting and aimlessness, well-being and unhappiness. And yet, why is it so hard to get motivated — or even if we do, to keep it up?

That is the question that scientists led by Professor Carmen Sandi at EPFL and Dr Gedi Luksys at the University of Edinburgh have sought to answer. The researchers worked off previous knowledge that told them two things: First, that people differ a lot in their capacity to engage in motivated behavior and that motivational problems like apathy are common in neurodegenerative and psychiatric disorders. Second, to target an area of the brain called the “nucleus accumbens”.

Sitting close to the bottom of brain, the nucleus accumbens has been the subject of a lot of research. The reason is that it was quickly found to be a major player in functions like aversion, reward, reinforcement, and motivation.

Antibody drug lowers risk of death in elderly COVID-19 patients: Cuban study

The 19 hospitalized patients from a single nursing home had tested positive for the virus in April.

All were older than age 64 and had chronic health conditions such as hypertension, dementia, heart disease, diabetes and lung diseases. Their age and health issues are considered risk factors for severe COVID-19.

The patients received either one or two intravenous doses of itolizumab along with the standard treatments used in Cuba at the time. Those included antiviral drugs, antibiotics, chloroquine, interferon, and blood thinners. Only two patients required oxygen therapy after the first dose, and all but one were discharged from the hospital in 14 days.

N”(Reuters) — An antibody drug already being used against the coronavirus in Cuba decreased the risk of intensive care admission and death among nursing home residents with moderate COVID-19, according to a small study conducted in the island nation.

India’s Biocon Ltd said earlier this month it received regulatory approval in India for itolizumab for use in coronavirus infected patients with moderate-to-severe respiratory distress. It was originally tested as a treatment for psoriasis.

Researchers, including from Cuba’s Center of Molecular Immunology, which developed itolizumab, said timely use of the drug in combination with standard therapy helped reduce inflammation and prevented COVID-19 from worsening.

Intercellular Adhesion Molecule-1 (ICAM-1) and ICAM-2 Differentially Contribute to Peripheral Activation and CNS Entry of Autoaggressive Th1 and Th17 Cells in Experimental Autoimmune Encephalomyelitis

Scientists from 4 different Swiss universities describe how adhesion molecules activate autoaggressive immune cells and drive their infiltration in the nervous system in a model of multiple sclerosis.

Click to read the paper published in Frontiers in Immunology: https://fro.ntiers.in/tp1U

In experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), myelin-specific T cells are activated in the periphery and differentiate in T helper (Th) 1 and Th17 effector cells, which cross the blood-brain barrier (BBB) to reach the central nervous system (CNS), where they induce neuroinflammation. Here, we explored the role of intercellular adhesion molecule-1 (ICAM-1) and ICAM-2 in the activation of naïve myelin-specific T cells and in the subsequent migration of differentiated encephalitogenic Th1 and Th17 cells across the BBB in vitro and in vivo. While on antigen-presenting cells ICAM-1, but not ICAM-2 was required for the activation of naïve CD4+ T cells, endothelial ICAM-1 and ICAM-2 mediated both Th1 and Th17 cell migration across the BBB. ICAM-1/-2-deficient mice developed ameliorated typical and atypical EAE transferred by encephalitogenic Th1 and Th17 cells, respectively. Our study underscores important yet cell-specific contributions for ICAM-1 and ICAM-2 in EAE pathogenesis.

Multiple sclerosis (MS) is considered an autoimmune inflammatory demyelinating disease of the central nervous system (CNS). Experimental autoimmune encephalomyelitis (EAE), a prototypic animal model for MS, mimics many aspects of the acute inflammatory phase of the human disease (1). In EAE, naïve myelin-reactive CD4+ T cells are activated and differentiated in peripheral lymphoid tissue into encephalitogenic Th1 or Th17 cells, which travel in the blood circulation to the CNS. After crossing the blood-brain barrier (BBB) they next infiltrate in the CNS parenchyma, leading to clinical manifestation of the disease (2). EAE can be actively induced by immunization with CNS myelin antigens emulsified in complete Freund’s adjuvant (aEAE) or by injection of myelin-reactive CD4+ T cells into syngeneic naïve recipients (tEAE) (3, 4).

Activation of naïve CD4+ T cells during aEAE occurs in the draining peripheral lymph nodes (dLNs), where T cells recognize their cognate antigen (Ag) on antigen-presenting cells (APCs) forming periodic contacts between the T-cell receptor (TCR) and the myelin oligodendrocyte glycoprotein (MOG)aa35−55 peptide loaded major histocompatibility complex (pMHC) on the APCs, referred to as the immunological synapse (IS) (5, 6). The fate of naïve T cells is determined within hours after Ag exposure by interacting with APCs in LN. The interaction between the integrin lymphocyte function associated antigen-1 (LFA-1) on the T cells and its ligand intercellular adhesion molecule-1 (ICAM-1) on the APCs is suggested to be involved in modulating the IS. However, APCs additionally express ICAM-2, an alternate ligand of LFA-1.

Putting on weight slows blood flow to the brain, increasing Alzheimer’s risk

COSTA MESA, Calif. – Health experts say around half of American adults are overweight or obese. While excessive body weight is linked to a number of serious health conditions, including diabetes and heart disease, a new study reveals it can also reduce blood flow to the brain. Researchers warn this can put overweight individuals at great risk for Alzheimer’s disease.

The study examines brain blood flow in 17,721 adults between 18 and 94. To do this, researchers use a brain imaging technique known as single photon emission computed tomography (SPECT).

SPECT is a technique in which doctors inject a radioactive tracer into a patient’s blood and then use a special camera to look at the flow of blood. Participants were then split into five categories: underweight, normal weight, overweight, obese, and morbidly obese — to examine blood flow in each of their brains. The brain scan data reveals lower blood flow across virtually all brain regions as body weight increases.

Inside the mind of an animal

Some neuroscientists are daring to wield the technologies to probe one powerful group of internal brain states: emotions. Others are applying them to states such as motivation, or existential drives such as thirst. Researchers are even finding signatures of states in their data for which they have no vocabulary.

Neuroscientists are scrutinizing huge piles of data to learn how brains create emotions and other internal states such as aggression and desire.

The Secret to a Long, Healthy Life Is in the Genes of the Oldest Humans Alive

The answer is in their genes—especially those that encode for basic life functions, such as metabolism. Thanks to the lowly C. elegans worm, we’ve uncovered genes and molecular pathways, such as insulin-like growth factor 1 (IGF-1) signaling that extends healthy longevity in yeast, flies, and mice (and maybe us). Too nerdy? Those pathways also inspired massive scientific and popular interest in metformin, hormones, intermittent fasting, and even the ketogenic diet. To restate: worms have inspired the search for our own fountain of youth.

Still, that’s just one success story. How relevant, exactly, are those genes for humans? We’re rather a freak of nature. Our aging process extends for years, during which we experience a slew of age-related disorders. Diabetes. Heart disease. Dementia. Surprisingly, many of these don’t ever occur in worms and other animals. Something is obviously amiss.

In this month’s Nature Metabolism, a global team of scientists argued that it’s high time we turn from worm to human. The key to human longevity, they say, lies in the genes of centenarians. These individuals not only live over 100 years, they also rarely suffer from common age-related diseases. That is, they’re healthy up to their last minute. If evolution was a scientist, then centenarians, and the rest of us, are two experimental groups in action.