Noor Biotech Institute - NBI

26/07/2026

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26/04/2026

19/01/2026

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01/05/2025

🔬✨ New Breakthrough in Antibiotic Discovery!

27/04/2025

Why Direct Astrocyte-to-Neuron Reprogramming Fails After Brain Hemorrhage
In a recent study published in Brain Hemorrhages, researchers explored whether the transcription factor Neurogenin2 (Ngn2) could reprogram astrocytes (supportive brain cells) into neurons after intracerebral hemorrhage (ICH) — a type of stroke caused by bleeding in the brain.

Here’s what they found:

In lab experiments (in vitro), Ngn2 could turn astrocytes into neuron-like cells under certain ideal conditions.

But when astrocytes were exposed to ICH-like damage (simulated with hemin), the reprogramming efficiency dropped significantly.

In living mice (in vivo) that suffered a brain hemorrhage, Ngn2 failed to induce astrocyte-to-neuron conversion altogether.

One major reason? After brain hemorrhage, microglia (the brain's immune cells) gobbled up the viral vectors carrying Ngn2 — preventing the reprogramming process.

Additionally, the harsh inflammatory environment after hemorrhage damaged the reprogramming potential.

🚧 Bottom line:
While Ngn2 has potential in controlled lab settings, it's not enough on its own to regenerate neurons after brain hemorrhage. Scientists now believe that multi-factor approaches or chemical reprogramming may be needed for future therapies.

🔗 Original study:
Chen S, Huang L, Wang J, et al. "Ngn2 failed to induce astrocyte-to-neuron reprogramming after intracerebral hemorrhage," Brain Hemorrhages (2025).

27/04/2025

🧠 METTL3: A New Player in Neurodegeneration?
A groundbreaking new study reveals that a key enzyme, METTL3, plays a central role in driving brain inflammation — especially in diseases like Parkinson’s Disease (PD), Alzheimer’s Disease (AD), and Dementia with Lewy Bodies (DLB).

When brain cells (microglia) are exposed to harmful substances like manganese (Mn) or the misfolded protein α-synuclein, METTL3 levels skyrocket.
Interestingly, the study showed that:

METTL3 moves out of the nucleus into the cytoplasm under stress.

It triggers the production of inflammatory molecules like TNF-α, IL-6, and IL-1β.

Knocking down METTL3 reduced inflammation, while overactivating it worsened brain inflammation.

Even more exciting, brain tissues from patients with PD and AD showed higher METTL3 levels compared to healthy individuals.

🧬 Researchers believe that targeting METTL3 could be a new therapeutic strategy to combat neurodegenerative diseases at their inflammatory roots.

Miller et al., "Pathological α-synuclein dysregulates epitranscriptomic writer METTL3 to drive neuroinflammation in microglia," Cell Reports (2025).

27/04/2025

Losing Our Edge: A Warning to America Spain gets it. They’re actively recruiting U.S. scientific talent, offering established researchers new opportunities to take their ideas, their labs, and their futures elsewhere. See for yourself: Spain’s Talent Consolidation Program https://lnkd.in/dBNYi5Y...

26/02/2025

CRISPR in Livestock

26/02/2025

Candida parapsilosis is persistent in a hospital environment hence it is often associated with nosocomial infections especially amongst low-birth weight neonates. Genetic modification is therefore important to characterise the physiological and virulence related properties of this fungus. A PCR-base...

26/02/2025

A roadmap toward genome-wide CRISPR screening throughout the organism

Genome-wide CRISPR screening in the organism has tremendous potential to answer long-standing questions of physiology and disease; however, technical limitations have prevented its broad application. Here, Fallon et al. highlight ongoing innovations in sgRNA delivery, library design, and phenotypic...