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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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The Hidden Impact: Lingering Brain Injury Symptoms Haunt Concussion Patients

Even mild concussion can cause long-lasting effects to the brain, according to researchers at the University of Cambridge. Using data from a Europe-wide study, the team has shown that for almost a half of all people who receive a knock to the head, there are changes in how regions of the brain commu

Activity-dependent protein synthesis in neurons requires microglial-metabolic coupling

During learning, the brain requires an exceptional amount of glucose to be imported into specific neural circuits, where it is used to form new memory-related proteins. Adler et al. discover that microglia, the resident immune cells of the brain, are critical for this process via a mechanism called microglial-metabolic coupling.

Full faces sharpen emotion recognition, even when eye details are blurred

A teary eye, a furrowed eyebrow, creases at the edge of the eye tell us what a person is feeling without them having to express it with words. New data indicate that eyes might be the window to the soul, but with curtains blocking half of their view, because the eyes alone do not contain enough information for our brain to derive emotions solely from them.

Researchers from the College of Wooster, USA, wanted to understand how much we actually rely on the eyes versus the whole face to recognize emotions. After examining participants’ brain activity using EEG (electroencephalography) as they viewed photographs of people displaying different emotions, they discovered that people can recognize emotions both more quickly and more accurately when they can see the entire face rather than just the eyes.

Blurring details in the eyes had little impact on people’s ability to recognize facial expressions as long as the rest of the face remained visible. When details in the eyes are reduced, the ability to read emotions takes a hit if the rest of the face is concealed, suggesting that the brain uses other features to fill in the gaps when information from the eyes is missing.

Alzheimer’s gene map expands to 91 loci, revealing 16 previously unknown risk regions

An international collaboration of genetic researchers has identified more than 90 genetic regions associated with the risk of Alzheimer’s disease and related dementias. The large-scale meta-analysis reveals new biological insights into the disease, highlighting the important roles of immune processes, beta-amyloid and tau biology, and lipid metabolism.

Alzheimer’s disease is the most common cause of dementia worldwide, and its development is influenced by a complex interplay of genetic and environmental factors. Understanding the genetic architecture of the disease is essential for improving diagnosis, risk prediction, and the development of targeted therapies.

In this study, researchers combined genome-wide association data from nearly a million individuals of European ancestry, including over 128,000 Alzheimer’s disease cases and nearly 850,000 controls.

Autism risk framework tracks genes, maternal factors and environment across 18,000 families

A new statistical framework developed by researchers at the Johns Hopkins Bloomberg School of Public Health, Johns Hopkins University School of Medicine, and Kaiser Permanente Northern California offers improved understanding of how genetics and environment contribute to autism risk.

Large-scale genetic studies have led to the development of genetic risk scores that estimate a person’s predisposition to diseases and health conditions based on their DNA profiles. The new framework allows researchers and clinicians to analyze these scores using family data and characterize the risk of conditions such as autism and other developmental conditions in children based on their own DNA, parental factors, and environmental influences such as maternal diet and lifestyle.

For their study published in Nature Genetics, the researchers analyzed more than 18,000 case-parent trios —autistic children and their parents—across diverse ancestral populations in the Simons Foundation Powering Autism Research for Knowledge consortium and the Genes and Environment Autism Research Study.

Biohybrid microrobots repair spinal cord by combining stem cells with magnetoelectric nanoparticles

Spinal cord injuries can have devastating consequences for those affected. Nerve cells in the spinal cord rarely regenerate naturally, while scarring often prevents the regrowth of nerve fibers. Modern therapies attempt to influence implanted stem cells using electrical stimulation to promote the growth of new nerve cells. This approach has several drawbacks: it requires implanted electrodes, and the transplanted cells do not always survive or integrate properly into the existing tissue.

Researchers in Zurich are pursuing a new approach, which they have published in the journal Nature Materials. This involves combining therapeutic stem cells with magnetoelectric nanoparticles in such a way that the cells can be guided magnetically to the precise site of an injury and stimulate the stem cells to accelerate repair.

To achieve this, the researchers created a biohybrid microrobot, which combines living neural progenitor cells (NPCs) with a technical component in the form of specially engineered nanoparticles.

Experimental Brain ‘Pacemakers’ May Rewire Circuits Linked to Depression

Every year, more than 2 million people in the United States are diagnosed with treatment-resistant depression.

Desperate for solutions, some brave patients are now volunteering to undergo surgery to place experimental ‘pacemakers’ into their brains.

These implanted electrodes are part of a treatment known as deep brain stimulation, which is currently used to address some cases of Parkinson’s disease and epilepsy.

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