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Conversely, neurotrophic treatment that revives neurons and rebuilds synapses and neurites shows a promise in slowing neurodegeneration. Pharmacological inhibitors that are purposed to reduce pathogenic factors have been unsuccessful in exerting a disease-modifying effect. Thus, it is of utmost urgency to find an effective treatment for neurodegenerative diseases. AD alone affects over 5 million people in the US and costs the US 100 billion dollars per year. As aged population grows very fast, the incidence of aging-related neurodegenerative diseases and their healthcare costs are increased exponentially.

Currently, there is no effective treatment for neurodegenerative diseases. Taken together, midi-GAGR with good BBB-permeability, long plasma half-life, and strong neuroprotective and neurotrophic effects has a great therapeutic potential for the treatment of neurodegenerative diseases, especially AD.Ĭonventional treatments for neurodegenerative diseases address only symptoms without disease-modifying effect but with serious side effects. Additionally, 14-day intranasal administration of midi-GAGR not only increased neuronal activity markers but also decreased hyperphosphorylated tau, a precursor of neurofibrillary tangle, in the brains of the AD mouse model, 3xTg-AD. Midi-GAGR appears to activate fibroblast growth factor receptor 1 (FGFR1) and its downstream neurotrophic signaling pathway for neuroprotection and CREB activation. Furthermore, intra-nasally administered midi-GAGR penetrated the BBB and exerted its neurotrophic effect inside the brain for 24 h after one-time administration. Moreover, midi-GAGR showed a good neurotrophic effect it enhanced neurite outgrowth and increased phosphorylated cAMP-responsive element binding protein (pCREB) in the nuclei of primary cortical neurons.

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Midi-GAGR protected rodent cortical neurons not only from the pathological concentrations of co-/post-treated free reactive radicals and Aβ 42 peptide but also from activated microglial cells. Midi-GAGR is a 4.7kD cleavage product of low acyl gellan gum that is approved by FDA for human use. Then, we discovered midi-GAGR, a BBB-permeable, long plasma half-life, strong neuroprotective and neurotrophic polysaccharide. Based on the recent findings of neuroprotective polysaccharides, we searched for a BBB-permeable neuroprotective polysaccharide among natural polysaccharides that are approved for human use. Thus, an alternative neurotrophic agent that has longer plasma half-life and better BBB-permeability has been sought for. However, the short plasma half-life and poor blood-brain-barrier (BBB)-permeability of neurotrophic peptides limit their in vivo efficacy. Among those, neurotrophic peptides that regenerate neuronal structures and increase neuron survival show a promise in slowing neurodegeneration. An enormous amount of efforts have been poured to find an effective therapeutic agent for the treatment of neurodegenerative diseases including Alzheimer’s disease (AD).