Author: Jean-Claude Muller, 穆卓Executive Editor at BtoBioInnovation email@example.com
SPECIAL REPORT #22.6
In 2016, Baroness Professor Susan Greenfield, from Oxford University, and a group of researchers at Neuro-Bio had published an article where they showed that T14, a C terminus fragment of the acetylcholinesterase (AChE) peptide is increased in Alzheimer’s disease brains and that its interaction with the α7-nAChR can elicit neurodegenerative-like events, such as reduction of neuronal activity and alteration of protein levels, including the nicotinic receptor itself, Aβ, APP, p-Tau, and GSK3. In the same article the authors demonstrated that T14 and the alpha-7 nicotinic receptor form a protein-protein complex and that this interaction could be reversed by NBP 14 a cyclized form of T14. NBP 14 occupies the same target than T14 and displaces the naturally occurring peptide form its protein-protein complex. NBP14 is the cyclized from of T4 which has the following amino-acid sequence: AEFHRWSSYMVHWK
This princeps findings opened the door for two hypotheses:
- Could T14 become an easy to follow valuable biomarker of Alzheimer’s disease?
- Could inactivation of T14 become a potential treatment of Alzheimer’s disease?
Six years later, the Neuro-Bio team, in collaboration with Evotec , UCLA and King’s College, London. has now shown, in a mouse model of Alzheimer’s disease, that both hypotheses are highly relevant. Following an intranasal treatment with NBP14 for six weeks resulted in marked decrease of brain amyloid and a treatment of 14 weeks improved cognitive performance comparable to that of normal mice.
In a press release of April 6, 2022, Baroness Professor Susan Greenfield, Founder and CEO of Neuro-Bio, said:
“By using basic neuroscientific knowledge, we have identified what we believe is a basic mechanism driving Alzheimer’s disease in the brain and have developed a molecule (NBP14) to combat it. Our recent efficacy study in mouse models further validates previous work describing an erstwhile unidentified mechanism in neurodegeneration and offers very exciting prospects for treating the disease in humans. This research should help position the drug intercepting this process, NBP14, for human clinical trials and hopefully create an entirely new era of Alzheimer’s therapeutics.”
Professor Paul L Herrling, former Global Head of Research of Novartis Pharma and Non-Executive Director at Neuro-Bio, said:
“The results consistently indicate that NBP14 might interfere with the neurotoxic process that leads to neuronal degeneration in Alzheimer’s. This work has very exciting implications for treating Alzheimer’s because it is based on a strong scientific theory that hasn’t yet been applied to treatment of the disease.”
The UK Medicines & Healthcare Products Regulatory Agency (MHRA) has granted NBP14 with one of their first “Innovation Passport”, a new regulatory pathway which allows faster clinical development.
The team also considers further studies aimed at demonstrating that regular measurements of T14 levels could be developed as blood test or a skin biopsy to follow the occurrence of the Alzheimer’s diseases neurodegenerative process over a period of ten to twenty years.
Neuro-Bio has plans to start a phase 1 clinical trial as soon as possible.
Although Neuro-Bio follows an attractive novel approach to test and treat Alzheimer’s disease, one should not underestimate the complexity of the disease which partially explains why, over two decades, the scientific and medical community have witnessed a vast number of failed clinical trials in the field.
Paris, April 7, 2022.
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