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Category: neuroscience

The Brain Health Accelerator Seeks to Revolutionize Neuroscience Research

For decades, researchers across institutions have peered into microscopes and dived into data to try to understand how diseases like Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS) affect the brain. While scientists have made many important insights into these conditions, breakthrough therapies to cure or even treat them remain out of reach.

To expedite understanding of and treatments for neurodegenerative diseases, the Allen Institute launched the Brain Health accelerator. The project, announced today, is a global initiative that will leverage cutting-edge technology with the goal of improving modeling, therapeutic development, and the understanding of disease mechanisms. With funding support from the Allen Institute, the Bezos family, Amazon Web Services, the National Institutes of Health, EverythingALS, and other partners, the project financial contribution is $400 million.

One of the challenges in studying diseases in the human brain and identifying treatment strategies has been the scale and complexity of the organ. The brain consists of many distinct parts, and studying disease mechanisms requires samples from large numbers of individuals. Additionally, while technological advancements in transcriptomics, proteomics, neuroimaging, and AI have helped researchers study the brain in finer detail, researchers have not always integrated many of these approaches into the same project.

Promising Anti-Aging Drug May Cause Brain Damage, Scientists Warn

The experimental drug combo dasatinib and quercetin (known for short as D+Q) is one of the most promising anti-aging therapies being developed right now.

It is not yet approved for human use, but some scientists think it has the potential to fight disease by improving how our systems clear out worn-down cells.

According to a new study, however, there might be a big problem with D+Q.

The delusion of a particle-only universe

If everything that happens in the world ultimately comes down to the behavior of fundamental particles, it would seem that other entities, from cells to human beings, from currencies to financial markets, aren’t really causing anything at all—that they are just shadows cast by patterns at the most fundamental level. But philosopher David Yates argues this conclusion is wrong. The whole affects the parts, and higher-level structures don’t just describe what is happening at lower levels in more convenient terms—they actively shape what is possible. This means that chemists, biologists, psychologists, and economists aren’t chasing shadows. They are studying structures that genuinely shape how the world unfolds.

In 1974, Jerry Fodor published a seminal paper titled ‘Special Sciences’, in which he argued for an intuitive and compelling picture of the relationship between fundamental physics and higher-level sciences such as biology, psychology and economics. Our world, according to Fodor, is arranged hierarchically, with fundamental physical particles at the bottom, combining to form molecules, which combine to form cells, which combine to form complex organisms, some of which have mental states, among them humans, who combine to form complex societies. The sciences are likewise arranged, with physics at the bottom, followed by chemistry, biology, physiology, neuroscience, psychology, sociology and economics. Now it is vanishingly unlikely, says Fodor, that things that share e.g. psychological or economic properties, also share some property specifiable in the language of physics or other lower-level sciences.

Embryonic transplantation and ischemic memory deficit

Transient forebrain ischemia is associated with selective neuronal vulnerability and persistent memory deficit. This study compares functional outcome and morphological changes in rats subjected to post-ischemic CA1 or hilus/dentate gyrus region hippocampal fetal transplantation. Ischemia was produced by bilateral common carotid artery occlusion with hypotension. Fetal hippocampal neurons were transplanted into both sides of the CA1 or hilus/dentate gyrus region of the dorsal hippocampus, 1 week post-ischemia. Four weeks post transplantation, the rats underwent behavioral testing for 5 consecutive days using the water maze trial. All animals were perfusion fixed for morphological studies. Transplants in the CA1 region of the dorsal hippocampus were associated with memory and morphological recovery, while grafts placed into the hilus/dentate gyrus region of the dorsal hippocampus were not. Similarly, neurons transplanted in the CA1 region of the dorsal hippocampus were morphologically similar to CA1 pyramidal cell neurons and stained positive with calbindin D(28k). In contrast the grafts transplanted into the hilus/dentate gyrus region of the dorsal hippocampus were morphologically heterogeneous and staining with calbindin D(28k) was not as robust. Post-ischemic transplantation in the CA1 region of the dorsal hippocampus is effective in improving memory and morphological function.

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Reappearance of hippocampal CA1 neurons after ischemia is associated with recovery of learning and memory

The pyramidal neurons of the hippocampal CA1 region are essential for cognitive functions such as spatial learning and memory, and are selectively destroyed after cerebral ischemia. To analyze whether degenerated CA1 neurons are replaced by new neurons and whether such regeneration is associated with amelioration in learning and memory deficits, we have used a rat global ischemia model that provides an almost complete disappearance (to approximately 3% of control) of CA1 neurons associated with a robust impairment in spatial learning and memory at two weeks after ischemia. We found that transient cerebral ischemia can evoke a massive formation of new neurons in the CA1 region, reaching approximately 40% of the original number of neurons at 90 days after ischemia (DAI). Co-localization of the mature neuronal marker neuronal nuclei with 5-bromo-2’-deoxyuridine in CA1 confirmed that neurogenesis indeed had occurred after the ischemic insult. Furthermore, we found increased numbers of cells expressing the immature neuron marker polysialic acid neuronal cell adhesion molecule in the adjacent lateral periventricular region, suggesting that the newly formed neurons derive from this region. The reappearance of CA1 neurons was associated with a recovery of ischemia-induced impairments in spatial learning and memory at 90 DAI, suggesting that the newly formed CA1 neurons restore hippocampal CA1 function. In conclusion, these results show that the brain has an endogenous capacity to form new nerve cells after injury, which correlates with a restoration of cognitive functions of the brain.

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