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Exercise Induces Adult Neurogenesis and Ameliorates Alzheimer’s Disease in Mice

A new study on adult neurogenesis and Alzheimer’s disease.


According to a study led by scientists at Massachusetts General Hospital, exercise-induced neurogenesis improves cognition in a mouse model of Alzheimer’s disease, yielding more benefits than drug-induced adult neurogenesis. The scientists were able to figure out the difference between the two types of induced neurogenesis and pharmacologically reproduce the same benefits provided by exercise [1].

Study abstract

Adult hippocampal neurogenesis (AHN) is impaired before the onset of Alzheimer’s disease (AD) pathology. We found that exercise provided cognitive benefit to 5×FAD mice, a mouse model of AD, by inducing AHN and elevating levels of brain-derived neurotrophic factor (BDNF). Neither stimulation of AHN alone, nor exercise, in the absence of increased AHN, ameliorated cognition. We successfully mimicked the beneficial effects of exercise on AD mice by genetically and pharmacologically inducing AHN in combination with elevating BDNF levels. Suppressing AHN later led to worsened cognitive performance and loss of preexisting dentate neurons. Thus, pharmacological mimetics of exercise, enhancing AHN and elevating BDNF levels, may improve cognition in AD. Furthermore, applied at early stages of AD, these mimetics may protect against subsequent neuronal cell death.

DARPA Wants Brain Interfaces for Able-Bodied Warfighters

The Next-Generation Nonsurgical Neurotechnology (N3) program will fund research on tech that can transmit high-fidelity signals between the brain and some external machine without requiring that the user be cut open for rewiring or implantation. It hasn’t escaped DARPA’s attention that no-surgery-required brain gear that gives people superpowers may find applications beyond the military. The proof-of-concept tech that comes out of the N3 program may lead to consumer products, says Justin Sanchez, director of DARPA’s Biological Technologies Office. “This will spawn new industries,” he says…


The N3 program will create no-surgery-required neurotech that the general public may also find useful.

Gene involved in circadian rhythms can be potential target for glioblastoma treatment

Researchers have discovered a way to kill #cancer cells and stop #glioblastoma formation by blocking casein kinase 1 gene.


Scientists with the Virginia Tech Carilion Research Institute say a gene involved in the body’s circadian rhythms is a potential target for therapies to help patients with a deadly form of brain cancer known as glioblastoma.

This discovery, to be published in the journal Scientific Reports on Tuesday, Sept. 11, points to a subtype of a particular gene that apparently is enabling the survival of cancer cells, although it is more commonly associated with circadian rhythms — the body’s 24-hour biological clock.

“The world is desperately seeking new treatments for glioblastoma and no one has ever before pointed to this gene as a target upon which to base therapies,” said Zhi Sheng, an assistant professor at the Virginia Tech Carilion Research Institute, whose team pinpointed the gene from 20 suspects it had previously identified.

One of the Most Famous Degenerative Diseases Affects the Brain in Previously Unknown Ways

An incurable affliction that gradually destroys a person’s ability to walk, speak, and eventually breathe can also deteriorate the mind, new research suggests. People with amyotrophic lateral sclerosis (ALS) are more likely to have other mental and behavioral health problems than people without the condition, the study found.

ALS, also called Lou Gehrig’s disease, is a progressive neurologic condition that affects some 20,000 Americans at any one time. In ALS, a person’s motor neurons throughout their body and brain steadily die off. These neurons are responsible for helping us carry out voluntary movement.

Digital government isn’t working in the developing world: Here’s why

The digital transformation of society has brought many immediate benefits: it’s created new jobs and services, boosted efficiency and promoted innovation. But when it comes to improving the way we govern, the story is not that simple.

It seems reasonable to imagine introducing digital information and communication technologies into public sector organisations – known as “digital ” or “e-government” – would have a beneficial impact on the way public services are delivered. For instance, by enabling people to claim rebates for medical bills via a government website.

When implemented well, e-government can reduce the cost of delivering government and public services, and ensure better contact with citizens – especially in remote or less densely populated areas. It can also contribute to greater transparency and accountability in public decisions, stimulate the emergence of local e-cultures, and strengthen democracy.

Life Extension Beyond Borders… — Life Extension Beyond Borders Association

Here in beautiful Basel, Switzerland we open the section Aging and Drug Discovery, actually an intersection of AI, longevity and drug discovery in the Innovation Forums of Basel Life Conference 2018. Dr Alex Zhavoronkov (InSilico Medicine) and Dr Morten Scheibye-Knudsen (University Copenhagen) welcomed us. Dr Jay Olshansky (University of Illinois at Chicago) gave the first lecture. Some examples for age face recognition were shown, emphasising the importance of wrinkles from smoking or others and suggesting that looking younger means living longer! After the wonderful lecture I immediately went to correct my make-up!

Molecule Appears to Have Anti-Aging Effects on the Vascular System

Β-hydroxybutyrate seems to prevent senescence of vascular tissue.


According to a study by Georgia State University scientists, a molecule called β-hydroxybutyrate has anti-aging effects on the vascular system; more specifically, the molecule appears to prevent senescence of vascular cells by promoting cellular quiescence instead [1].

Study abstract

β-hydroxybutyrate (β-HB) elevation during fasting or caloric restriction is believed to induce anti-aging effects and alleviate aging-related neurodegeneration. However, whether β-HB alters the senescence pathway in vascular cells remains unknown. Here we report that β-HB promotes vascular cell quiescence, which significantly inhibits both stress-induced premature senescence and replicative senescence through p53-independent mechanisms. Further, we identify heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) as a direct binding target of β-HB binding to hnRNP A1 markedly enhances hnRNP A1 binding with Octamer-binding transcriptional factor Oct4 mRNA, which stabilizes Oct4 mRNA and Oct4 expression. Oct4 increases Lamin B1, a key factor against DNA damage-induced senescence. Finally, fasting and intraperitoneal injection of β-HB upregulate Oct4 and Lamin B1 in both vascular smooth muscle and endothelial cells in mice in vivo.

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