A new approach
Neuro-Bio drug reversed Alzheimer's disease in mice
Publishing work in Alzheimer's & Dementia: Translational Research & Clinical Interventions (Greenfield et al., A novel process driving Alzheimer's disease validated in a mouse model: Therapeutic potential), Neuro-Bio researchers in collaboration with drug development company Evotec SE, University of California at Los Angeles and King's College London They studied the ability of their patented drug NBP14 to fight neurodegeneration in a mouse model of Alzheimer's disease.
Intranasal treatment for 6 weeks led to a noticeable decrease in the level of amyloid in the brain, and after 14 weeks – to an improvement in cognitive functions to indicators comparable to those in normal mice. The results highlight the effectiveness of the Neuro-Bio candidate drug and represent a significant step forward towards the treatment of Alzheimer's disease in humans.
Baroness Professor Susan Greenfield, founder and CEO of Neuro-Bio, says: "Using basic neurobiological knowledge, we identified what we believe is the main mechanism causing Alzheimer's disease in the brain and developed a molecule (NBP14) to combat it. Our recent efficacy study in mouse models once again confirms previous work describing a hitherto unidentified neurodegeneration process and offers very interesting prospects for the treatment of this disease in humans. This study should help position the drug intercepting this process, NBP14, for human clinical trials and, hopefully, will open a whole new era of therapy for Alzheimer's disease."
Professor Paul L. Herrling, former head of global research at Novartis Pharma and non-executive director of Neuro-Bio, says: "The results consistently indicate that NBP14 may interfere with the neurotoxic process that leads to neuron degeneration in Alzheimer's disease. This work has very interesting implications for the treatment of Alzheimer's disease, because it is based on a strong scientific theory that has not yet been applied to the treatment of this disease."
The UK regulatory body, the Medicines and Healthcare Products Regulatory Agency, has accredited NBP14 as one of its first "Innovation Passports" under a new licensing mechanism aimed at reducing the time to market for innovative medicines.
NBP14 works by intercepting a process that, according to Neuro-Bio, may be the main driving force of neurodegeneration, the action of a brain chemical called T14 [1, 2]. Over the past twenty years since it was first identified [3], evidence that T14 plays an important role in early cell growth and normal development are becoming increasingly convincing. However, this action can become toxic if it is caused improperly in adulthood [4], and can eventually lead to Alzheimer's disease, in which T14 levels in the brain, as shown in the current article, reflect the degree of degeneration.
Inactivation of T14 could potentially serve as a treatment for Alzheimer's disease by stopping the early development of cell damage occurring first in the most vulnerable cells deep in the brain. Originally identified by neurologist Martin Rossor back in 1981 [5], these primarily vulnerable cells form a kind of central node in the brain extending upwards from the tip of the spinal cord. The key feature is that they are the first to show pathology at an early stage of neurodegeneration [6].
Neuro-Bio believes that the detection and measurement of T14 can be developed using a blood test or a skin biopsy to detect the occurrence of a degenerative process over a period of ten to twenty years, which usually occurs before the onset of symptoms. If NBP14 proves effective in human trials, it could become a common nasal spray for home use to stop neurodegeneration before any symptoms appear.
No harmful side effects at the active dose were observed during the study of the effectiveness of NBP14 in the disease model. Neuro-Bio Company plans to start clinical trials of the first phase as soon as possible.
Dr. Gregory Cole, professor of medicine and neurology at UCLA and associate director of the UCLA Alzheimer's Disease Center, says: "I specialize in Alzheimer's disease research and have been working on a real treatment within the UCLA Alzheimer's Program since 1994. Together with my colleagues around the world, we have all witnessed hundreds of failed drug trials based on existing theories, and we are ready for truly new approaches. NBP14 has clear advantages over other candidate drugs, and I am happy to work with this team at Neuro-Bio and share their success."
Links:
[1] Garcia-Rates S, Morrill P, Tu H, Pottiez G, Badin AS, Tormo-Garcia C, et al. (I) Pharmacological profiling of a novel modulator of the alpha7 nicotinic receptor: Blockade of a toxic acetylcholinesterase-derived peptide increased in Alzheimer brains. Neuropharmacology. 2016;105:487-99.
[2] Brai E, Simon F, Cogoni A, Greenfield SA. Modulatory Effects of a Novel Cyclized Peptide in Reducing the Expression of Markers Linked to Alzheimer’s Disease. Front Neurosci. 2018;12:362.
[3] Greenfield S, Vaux DJ. Parkinson’s disease, Alzheimer’s disease and motor neurone disease: identifying a common mechanism. Neuroscience. 2002;113:485-92.
[4] Day T, Greenfield SA. Bioactivity of a peptide derived from acetylcholinesterase in hippocampal organotypic cultures. Exp Brain Res. 2004;155:500-8.
[5] Rossor MN. Parkinson’s disease and Alzheimer’s disease as disorders of the isodendritic core. Br Med J (Clin Res Ed). 1981;283:1588-90.
[6] Theofilas P, Dunlop S, Heinsen H, Grinberg LT. Turning on the Light Within: Subcortical Nuclei of the Isodentritic Core and their Role in Alzheimer’s Disease Pathogenesis. J Alzheimers Dis. 2015;46:17-34.
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