Study summary · research use only
Rescue of cognitive-aging by administration of a neurogenic and/or neurotrophic compound
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this study, the authors administered peptide 021 (P021), a small neurotrophic compound derived from ciliary neurotrophic factor, orally to 22 to 24-month-old Fisher rats. The abstract reports that chronic P021 significantly reduced age-dependent decline in learning and memory, inhibited the deficit in neurogenesis in aged rats, increased brain-derived neurotrophic factor expression, and restored synaptic deficits in cortex and hippocampus. Using in vivo magnetic resonance spectroscopy, it reports age-dependent changes in hippocampal metabolites and that P021 significantly reduced myoinositol concentration, which was increased in aged versus young rats. The authors describe P021 as a promising compound for cognitive aging.
Abstract
Aging is characterized by a progressive decline of cognitive performance, which has been partially attributed to structural and functional alterations of hippocampus. Importantly, aging is the major risk factor for the development of neurodegenerative diseases, especially Alzheimer's disease. An important therapeutic approach to counteract the age-associated memory dysfunctions is to maintain an appropriate microenvironment for successful neurogenesis and synaptic plasticity. In this study, we show that chronic oral administration of peptide 021 (P021), a small peptidergic neurotrophic compound derived from the ciliary neurotrophic factor, significantly reduced the age-dependent decline in learning and memory in 22 to 24-month-old Fisher rats. Treatment with P021 inhibited the deficit in neurogenesis in the aged rats and increased the expression of brain derived neurotrophic factor. Furthermore, P021 restored synaptic deficits both in the cortex and the hippocampus. In vivo magnetic resonance spectroscopy revealed age-dependent alterations in hippocampal content of several metabolites. Remarkably, P021 was effective in significantly reducing myoinositol (INS) concentration, which was increased in aged compared with young rats. These findings suggest that stimulating endogenous neuroprotective mechanisms is a potential therapeutic approach to cognitive aging, Alzheimer's disease, and associated neurodegenerative disorders and P021 is a promising compound for this purpose.
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