Lifeboat Foundation: Safeguarding Humanity
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Gene therapy and correction can be used in almost all diseases and pathological conditions because of recent advancements, but some questions still have yet to be answered in this field of advancement. Based on the requirements and compatibility, gene therapy is divided into two parts: somatic gene therapy and germline gene therapy. If the transfer of DNA segments is done to cells that will affect the next generation, this is called somatic gene therapy. Somatic gene therapy is currently more efficient in research due to its less ethical issue and less complexity. The toughest task for curing diabetes with gene therapy is to have glucose responsiveness to insulin transgene expression. So studies were carried out to decrease obesity by gene therapy to decrease type 2 diabetes prevalence. Gene therapy using viral vectors remains risky and is still under scrutiny to ensure safety and efficacy during clinical trials.

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Brain organoids are self-organizing tissue cultures grown from patient cell-derived induced pluripotent stem cells. They form tissue structures that resemble the brain in vivo in many ways. This makes brain organoids interesting for studying both normal brain development and for the development of neurological diseases. However, organoids have been poorly studied in terms of neuronal activity, as measured by electrical signals from the cells.

A team of scientists led by Dr. Thomas Rauen from the Max Planck Institute for Molecular Biomedicine in Münster, Germany, in collaboration with Dr. Peter Jones’ group at the NMI (Natural and Medical Sciences Institute at the University of Tübingen, Germany), has now developed a novel microelectrode array system (Mesh-MEA) that not only provides optimal growth conditions for human , but also allows non-invasive electrophysiological measurements throughout the entire growth period. This opens up new perspectives for the study of various brain diseases and the development of new therapeutic approaches.

The study is published in the journal Biosensors and Bioelectronics.

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Researchers at Rutgers and Emory University are gaining insights into how schizophrenia develops by studying the strongest-known genetic risk factor.

When a small portion of chromosome 3 is missing—known as 3q29 deletion syndrome—it increases the risk for by about 40-fold.

Researchers have now analyzed overlapping patterns of altered gene activity in two models of 3q29 deletion syndrome, including mice where the deletion has been engineered in using CRIPSR, and , or three-dimensional tissue cultures used to study disease. These two systems both exhibit impaired . This dysfunction can cause energy shortfalls in the brain and result in psychiatric symptoms and disorders.

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