The Stem Cell Reports paper demonstrated the capability to grow and differentiate cortical neurons — known to be responsible for a majority of higher brain function — into fully mature and functional cells.

These neurons were then incorporated into a circuit functioning as a simulated system, where the researchers were able to induce long-term potentiation (LTP). LTP — which allows for memory formation — is a key phenomenon in the study of cognition, and one that has mostly evaded direct observation in human models.

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A UCF researcher’s work to create a “brain-on-a-chip” aims to improve neurological disorder research by speeding up drug discovery and providing an alternative to animal testing.

James Hickman — professor of chemistry, biomolecular sciences and electrical engineering — recently published some of his latest findings in the journals Stem Cell Reports and Advanced Therapeutics.

These studies explain advancements in his research group’s efforts to develop the functional neural model otherwise known as a “brain-on-a-chip.” Such a model could revolutionize neurological research by replicating the pathologies of neurological disorders and rare autoimmune neuropathies, without the need for testing on human or animal subjects.

Most treatments for strokes aim to help reduce or repair damage to affected neurons. But a new study in mice has shown that a drug already in use to treat certain neurological disorders could help patients recover from strokes by getting undamaged neurons to pick up the slack.

An ischemic stroke occurs when a blood vessel blockage interrupts blood flow to the brain, causing neurons to die off. Survivors can suffer impaired fine motor control and speech, and other disabilities, for which long-term rehabilitation is often required.

Logically, many treatment options in development focus on minimizing or reversing damage to neurons, using things like stem cells, anti-inflammatory drugs, injectable hydrogels, or molecules that convert neighboring cells into neurons.

Repression of the G protein-coupled chemokine receptor CCR5 enhances MAPK/CREB signaling, long-term potentiation, somatosensory cortical plasticity, and learning and memory, while CCR5 over-activation by viral proteins may contribute to HIV-associated cognitive deficits.

𝙏𝙝𝙚 𝙘𝙤𝙣𝙙𝙞𝙩𝙞𝙤𝙣𝙨 𝙘𝙖𝙣 𝙖𝙡𝙡 𝙖𝙛𝙛𝙚𝙘𝙩 𝙩𝙝𝙚 𝙗𝙧𝙖𝙞𝙣, 𝙙𝙖𝙢𝙖𝙜𝙞𝙣𝙜 𝙗𝙡𝙤𝙤𝙙 𝙫𝙚𝙨𝙨𝙚𝙡𝙨 𝙖𝙣𝙙 𝙡𝙚𝙖𝙙𝙞𝙣𝙜 𝙩𝙤 𝙨𝙩𝙧𝙤𝙠𝙚𝙨. 𝘽𝙪𝙩 𝙩𝙝𝙚 𝙘𝙤𝙣𝙣𝙚𝙘𝙩𝙞𝙤𝙣 𝙗𝙚𝙩𝙬𝙚𝙚𝙣 𝙫𝙖𝙨𝙘𝙪𝙡𝙖𝙧 𝙙𝙞𝙨𝙚𝙖𝙨𝙚 𝙞𝙣 𝙩𝙝𝙚 𝙗𝙧𝙖𝙞𝙣 𝙖𝙣𝙙 𝘼𝙡𝙯𝙝𝙚𝙞𝙢𝙚𝙧’𝙨 𝙝𝙖𝙨 𝙧𝙚𝙢𝙖𝙞𝙣𝙚𝙙 𝙪𝙣𝙚𝙭𝙥𝙡𝙖𝙞𝙣𝙚𝙙 𝙙𝙚𝙨𝙥𝙞𝙩𝙚 𝙩𝙝𝙚 𝙞𝙣𝙩𝙚𝙣𝙨𝙚 𝙚𝙛𝙛𝙤𝙧𝙩𝙨 𝙤𝙛 … See more.

The Neuro-Network.

𝐑𝐞𝐬𝐞𝐚𝐫𝐜𝐡𝐞𝐫𝐬 𝐦𝐚𝐲 𝐡𝐚𝐯𝐞 𝐟𝐨𝐮𝐧𝐝 𝐭𝐡𝐞 𝐦𝐢𝐬𝐬𝐢𝐧𝐠 𝐥𝐢𝐧𝐤 𝐛𝐞𝐭𝐰𝐞𝐞𝐧 𝐀𝐥𝐳𝐡𝐞𝐢𝐦𝐞𝐫’𝐬 𝐚𝐧𝐝 𝐯𝐚𝐬𝐜𝐮𝐥𝐚𝐫 𝐝𝐢𝐬𝐞𝐚𝐬𝐞

𝙁𝙤𝙧 𝙢𝙤𝙧𝙚 𝙩𝙝𝙖𝙣 20 𝙮𝙚𝙖𝙧𝙨, 𝙨𝙘𝙞𝙚𝙣𝙩𝙞𝙨𝙩𝙨 𝙝𝙖𝙫𝙚 𝙠𝙣𝙤𝙬𝙣 𝙩𝙝𝙖𝙩 𝙥𝙚𝙤𝙥𝙡𝙚 𝙬𝙞𝙩𝙝 𝙝𝙮𝙥𝙚𝙧𝙩𝙚𝙣𝙨𝙞𝙤𝙣… See more.

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For more than 20 years, scientists have known that people with hypertension, diabetes, high cholesterol, or obesity have a higher likelihood of developing Alzheimer’s disease.

The conditions can all affect the brain, damaging blood vessels and leading to strokes. But the connection between vascular disease in the brain and Alzheimer’s has remained unexplained despite the intense efforts of researchers.

Summary: Study reveals the ZNF117 gene is a major regulator of glioblastoma tumor cells.

Source: Yale.

A recent research paper published in Nature Communications by a team led by Yale School of Medicine researchers finds a promising way to make brain cancer cells more susceptible to chemotherapy.