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Engineered immune therapy could help fight brain aging

Researchers at Stanford University engineered a modified version of the immune protein interleukin-10 (IL-10) that retains only its anti-inflammatory properties while eliminating its pro-inflammatory ones. When injected into aged mice, this modified protein stimulated the growth of new neurons and improved performance on memory and learning tasks, such as maze navigation and object recognition. The study, published in Immunity, suggests that age-related cognitive decline is linked to the accumulation of exhausted T-lymphocytes in the brain, chronic inflammation, and impaired microglial function — all of which reduce neurogenesis. The findings indicate that selectively modulating immune signaling could open new avenues for treating neurodegenerative diseases. The team plans to further investigate the protein’s mechanisms and explore ways to target specific cell types more precisely to minimize potential side effects.


A modified immune protein developed by Stanford researchers points to a novel strategy for combating age-related cognitive decline.

The Nervous System and Behavior

Many central issues with which neurosciences is concerned, such as how we perceive the world around us, how we learn from experience, how we remember, how we direct our movements, and how we communicate with each other, have commanded the attention of thoughtful men and women for centuries. But it was not until after World War II that neuroscience began to emerge as a separate and increasingly vigorous scientific discipline that has as its ultimate objective providing a satisfactory account of animal (including human) behavior in biological terms. This ambitious goal has as its basis the central realization that all behavior is, in the last analysis, a reflection of the function of the nervous system. It is the organized and coordinated activity of the nervous system that ultimately manifests itself in the behavior of the organism. The challenge to neuroscience then, is to explain, in physical and chemical terms, how the nervous system marshalls its signaling units to direct behavior.

The real magnitude of this challenge can perhaps be best judged by considering the structural and functional complexity of the human brain and the bewildering complexity of human behavior. The human brain is thought to be composed of about a hundred billion (1011) nerve cells and about 10 to 50 times that number of supporting elements or glial cells. Some nerve cells have relatively few connections with other neurons or with such effector organs as muscles or glands, but the great majority receive connections from thousands of other cells and may themselves connect with several hundred other neurons. This means that at a fairly conservative estimate the total number of functional connections (known as synapses) within the human brain is on the order of a hundred trillion (1014). But what is most important is that these connections are not random or indiscriminate:

They constitute the essential “wiring” of the nervous system on which the extraordinarily precise functioning of the brain depends. We owe to the great neuroanatomists of the last century, and especially to Ramón y Cajal, the brilliant insight that cells with basically similar properties are able to produce very different actions because they are connected to each other and to the sensory receptors and effector organs of the body in different ways. One major objective of modern neuroscience is therefore to unravel the patterns of connections within the nervous system—in a word, to map the brain.

Interferons: Interferons (IFNs) are a family of antiviral and immunomodulatory signaling proteins produced by host cells to fight pathogens like viruses, bacteria, and tumors

(IFNs) are a family of antiviral and immunomodulatory signaling proteins produced by host cells to fight pathogens like viruses, bacteria, and tumors.

As cytokines, they alert neighboring cells to activate defenses, inhibit viral replication, and regulate immune responses.

Common uses include treating hepatitis B and C, multiple sclerosis, and certain cancers like melanoma and lymphoma.

For more information click on the link below: sciencenewshighlights ScienceMission.

Why you can’t tie knots in four dimensions

We all know we live in three-dimensional space. But what does it mean when people talk about four dimensions? Is it just a bigger kind of space? Is it “space-time,” the popular idea which emerged from Einstein’s theory of relativity?

If you have wondered what four dimensions really look like, you may have come across drawings of a “four-dimensional cube.” But our brains are wired to interpret drawings on flat paper as two-or at most three-dimensional, not four-dimensional.

The almost insurmountable difficulty of visualizing the fourth dimension has inspired mathematicians, physicists, writers and even some artists for centuries. But even if we can’t quite imagine it, we can understand it.

DEGS1-Related Hypomyelinating LeukodystrophyFour Individuals From Same Family and Review of Literature

Degs1-related hypomyelinating leukodystrophy: four individuals from same family and review of literature.


ObjectivesDEGS1-related leukodystrophy has been described in 33 individuals to date with varying degrees of neurologic symptoms and atrophy/hypomyelination on MRI brain. We describe a family of 4 individuals with DEGS1-related leukodystrophy with phenotypic heterogeneity both within the family and in previously reported individuals.

Management of Inherited CNS Small Vessel Diseases: The CADASIL Example: A Scientific Statement From the American Heart Association

Lacunar infarcts and vascular dementia are important phenotypic characteristics of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, the most common inherited cerebral small vessel disease. Individuals with the disease show variability in the nature and onset of symptoms and rates of progression, which are only partially explained by differences in pathogenic mutations in the NOTCH3 gene. Recognizing the disease early in its course and securing a molecular diagnosis are important clinical goals, despite the lack of proven disease-modifying treatments.

Frequently distracted? Your brain rhythms may be to blame

Scientists may have new answers to why pop-ups or notifications grab our attention. Turns out our attention is on a cycle, shifting seven to 10 times per second. This rhythmic occurrence may be crucial for survival, as it prevents us from becoming overly focused on one thing in our environment. It could help us to see a car backing up in a parking lot while we search for where we parked, or to duck to avoid a low-hanging tree branch on a walk while watching a kid ride a bike.

However, these windows that shift our attention could also make us more susceptible to distractions, especially in modern times. As we live in a world surrounded by screens, digital alerts, and other visual stimuli, these frequent and innate windows for shifting attention may make it easier to be pulled away from a task.

“For our ancestors who had to continue to monitor the environment for predators while foraging for food, this was a beneficial trait,” said Ian Fiebelkorn, Ph.D., assistant professor of Neuroscience at the Del Monte Institute for Neuroscience at the University of Rochester and senior author of a study out in the journal PLOS Biology. “But in our modern environment, with laptops open in front of us and a smartphone nearby, rhythmically occurring windows for beneficial attentional shifts might also work against us. That is, rhythmically occurring windows for attentional shifts are also associated with increased susceptibility to distracting information.”

Is The Brain an Analog Computer? Consciousness as Dynamic Brainwave Organization | Earl Miller

Professor Earl Miller discusses, Mind-Body Solution podcast.

Earl K. Miller is the Picower Professor of Neuroscience at the Massachusetts Institute of Technology. He has faculty positions in The Picower Institute for Learning and Memory and the Department of Brain and Cognitive Sciences. He holds degrees from Kent State University (B.A.) and Princeton University (M.A., Ph.D.) as well as an honorary Doctor of Science from Kent State University.


For decades, neuroscience treated the brain like a digital machine — storing information in synaptic connections and sustaining activity like a switch flipped on. But what if that model is incomplete?

In this conversation, I sit down with Earl Miller, MIT professor and head of the Miller Lab, to explore a growing shift in cognitive neuroscience: the brain may compute using dynamic electrical waves.

We discuss how oscillations coordinate millions of neurons, how waves interact with spikes in a two-way system, why large-scale brain organization may depend on rhythmic patterns, and what this means for artificial intelligence.

Tumor-immune-neural circuit disrupts energy homeostasis in cancer cachexia

Tumor-immune-neural circuit in cancer cachexia.

The mechanisms involved in cancer-mediated cachexia and anorexia are not well understood.

The researchers in this study delineate an interplay among tumor cells, immune cells, and the nervous system that drives cancer cachexia and anorexia.

The authors show thay loss of GDF15 protects against appetite loss, muscle wasting, and fat loss in pancreatic, lung, and skin cancers.

Disrupting this feedforward loop with GDF15-neutralizing antibody, anti-CSF1R antibody, or Rearranged during Transfection (RET) inhibitor alleviates cachexia and anorexia across cancer models. sciencenewshighlights ScienceMission https://sciencemission.com/Tumor-immune-neural-circuit


Shi et al. delineate an interplay among tumor cells, immune cells, and the nervous system that drives cancer cachexia and anorexia. Specifically, tumor-derived CSF1 induces macrophage GDF15, which signals through the GFRAL-RET neural axis to enhance β-adrenergic activity and systemic wasting. Disrupting this feedforward loop alleviates cachexia across cancer models.

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