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Elevated Tau Level in Aged Rat Cerebrospinal Fluid Reduced by Treatment with a Neurotrophic Compound
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this study, the authors examined a neurotrophic compound (DGGLAG, named P021) in aged Fisher rats as a model of cerebral aging. The abstract reports that P021 is blood-brain-barrier-permeable and that chronic oral treatment reduced brain total tau in aged rats. It states cerebrospinal fluid levels of both tau and Abeta/AbetaPP were elevated in aged animals and that chronic P021 treatment reduced tau, but not Abeta/AbetaPP, toward levels found in young adult rats, without inducing a detectable immune reaction. The authors describe P021's therapeutic potential as a disease-modifying compound and the aged Fisher rats as a model for monitoring a tau-reducing compound in cerebrospinal fluid.
Abstract
Alzheimer's disease (AD) is the single major cause of dementia in middle- to old-age individuals, and, as of yet, no disease-modifying therapeutic drug is available for its treatment. A major obstacle in the successful development of disease-modifying therapeutic drugs has been the lack of suitable animal models of the sporadic form of AD as well as a biomarker that can be used both for therapeutic preclinical studies and for human clinical trials. Previously we showed neurogenesis and neuronal plasticity deficits and cognitive impairment and their rescue with a neurotrophic peptidergic compound, DGGLAG named P021, in aged Fisher rats. Here we show that P021 is blood-brain-barrier-permeable, and chronic oral treatment with this compound can reduce the brain level of total tau in the aged rats. Furthermore, cerebrospinal fluid (CSF) levels of both tau and Aβ/AβPP are elevated in the aged animals, and chronic treatment with P021 can reduce tau but not Aβ/AβPP to that of the levels found in young adult rats. Importantly, P021 does not induce any detectable immune reaction in rats. Collectively, these studies show the therapeutic potential of P021 as a disease-modifying compound and the suitability of the aged Fisher rats as a model of cerebral aging in which the therapeutic efficacy of a tau-reducing compound can be monitored in the CSF.
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