Noor Biotech Institute - NBI

Noor Biotech Institute - NBI At Noor Biotech Institute (NBI), we are dedicated to fostering cutting-edge research, academic excellence, and innovative scientific discoveries.

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26/04/2026
19/01/2026

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🔬✨ New Breakthrough in Antibiotic Discovery!
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.

đźš§ 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.

đź”— 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

đź§  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...

A roadmap toward genome-wide CRISPR screening throughout the organism
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...

Making Gene Therapy Faster And Better With Fuse Vectors
26/02/2025

Making Gene Therapy Faster And Better With Fuse Vectors

Fuse Vectors has raised $5.2 million of funding as it moves closer to commercialising its innovative new approach to manufacturing gene therapies

Unlocking the Secrets of Aging: How Environment and Genetics Shape Our LifespanAging is one of life's few certainties, b...
24/02/2025

Unlocking the Secrets of Aging: How Environment and Genetics Shape Our Lifespan

Aging is one of life's few certainties, but how exactly do we age, and why do some of us experience faster or more pronounced aging than others? A groundbreaking study has taken a deep dive into this question, offering some eye-opening answers about the combined role of genetics and environmental factors in shaping our aging process and mortality.
The Exposome: More Than Just Genetics

For years, we’ve known that genetics plays a significant role in determining how we age. But what about the environment around us? The exposome—essentially, the total set of environmental exposures we encounter throughout our lives—is emerging as a crucial factor influencing aging and health. This new research, based on an extensive analysis of over 490,000 participants from the UK Biobank, reveals that environmental factors might just have a larger impact on aging than previously thought, possibly even outweighing genetic influences.
Key Findings: Environment Drives Aging

Exposome vs. Genetics: The study found that environmental factors explained a stunning 17% more of the variation in mortality compared to genetic risk scores for major diseases. In simple terms, the environment (our lifestyle, socioeconomic status, physical activity, sleep habits, etc.) has a stronger influence on how we age and whether we live a long life than our genes alone.

The 25 Deadly Exposures: The research pinpointed 25 environmental factors—ranging from smoking and physical activity levels to socioeconomic status and even childhood body size—that are independently linked to both premature death and biological aging. Many of these factors are modifiable, meaning we have the power to influence them and, in turn, affect our aging process.

Proteomic Age Clock: The study used a cutting-edge method known as the proteomic age clock, which looks at the proteins in our blood to determine how biologically old we are compared to our actual age. The results? Environmental exposures such as smoking, sleep patterns, and physical activity are closely tied to how fast our bodies age at the cellular level.

The Role of Genetics: A Smaller Piece of the Puzzle

While the study highlights the importance of environmental factors, it doesn't disregard genetics. Polygenic risk scores (PRS) that assess genetic predisposition to certain diseases—such as cancer, Alzheimer’s, and heart disease—are still important, but their contribution to aging and mortality is smaller than the combined influence of the exposome. For certain diseases like cancer and dementia, genetic factors play a larger role, but for conditions like lung disease, liver disease, and heart disease, the environment is the dominant factor.
Why Does This Matter?

This research has huge implications for public health and aging. It challenges the notion that we are simply victims of our genes, and instead places a strong emphasis on the power of environmental and lifestyle changes. If we can manage environmental exposures—by quitting smoking, increasing physical activity, improving sleep, and addressing social determinants of health like income and living conditions—we could significantly delay aging and increase life expectancy.
What Can We Do About It?

This study serves as a call to action for both individuals and policymakers. For individuals, making small but impactful lifestyle changes like exercising more, reducing smoking, and managing stress could make a world of difference. On a larger scale, public health initiatives that focus on improving socioeconomic conditions and providing access to healthier environments could be key in tackling the aging epidemic.
Conclusion: A Future Where We Age Better

By unlocking the complex relationship between our genes and the environment, this study offers us a roadmap for healthier aging. With an increased understanding of the exposome, we can start making informed decisions to extend our healthspan and live longer, better lives. So, the next time you think about aging, remember—it’s not just about the genes you were born with, but also the environment you create for yourself along the way.

The original research can be reached at the link

Based on a systematic analysis of environmental exposures associated with aging and mortality in the UK Biobank, the relative contributions of such exposures and genetic risk for mortality and a range of age-related diseases were compared, highlighting the potential beneficial effects of environment...

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