Study summary · research use only
Alzheimer's Disease: Challenges and a Therapeutic Opportunity to Treat It with a Neurotrophic Compound
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This review discusses Alzheimer's disease (AD) pathology in humans, including deficits in neurogenesis and synaptic plasticity linked to neurofibrillary tau and amyloid β pathology and neuroinflammation, and an imbalance of neurotrophic factors (increased FGF-2, decreased BDNF and neurotrophin 4) in the hippocampus, frontal cortex, and parietal cortex. It notes prior attempts to use neurotrophic factors as AD treatments were halted due to blood-brain barrier impermeability, short half-life, and severe side effects. The review focuses on the small neurotrophic and neurogenic peptide mimetic compound P021, discovered by the authors' laboratory, describing pre-clinical studies and its potential as a therapeutic candidate for AD and related neurodegenerative disorders, while noting the review's scope is limited to P021 and related literature.
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disease with an insidious onset and multifactorial nature. A deficit in neurogenesis and synaptic plasticity are considered the early pathological features associated with neurofibrillary tau and amyloid β pathologies and neuroinflammation. The imbalance of neurotrophic factors with an increase in FGF-2 level and a decrease in brain derived neurotrophic factor (BDNF) and neurotrophin 4 (NT-4) in the hippocampus, frontal cortex and parietal cortex and disruption of the brain micro-environment are other characteristics of AD. Neurotrophic factors are crucial in neuronal differentiation, maturation, and survival. Several attempts to use neurotrophic factors to treat AD were made, but these trials were halted due to their blood-brain barrier (BBB) impermeability, short-half-life, and severe side effects. In the present review we mainly focus on the major etiopathology features of AD and the use of a small neurotrophic and neurogenic peptide mimetic compound; P021 that was discovered in our laboratory and was found to overcome the difficulties faced in the administration of the whole neurotrophic factor proteins. We describe pre-clinical studies on P021 and its potential as a therapeutic drug for AD and related neurodegenerative disorders. Our study is limited because it focuses only on P021 and the relevant literature; a more thorough investigation is required to review studies on various therapeutic approaches and potential drugs that are emerging in the AD field.
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