ArticleCNS neuroscience & therapeutics2026
Intranasal Administration of an Arginine-Enriched Penetratin Peptide Confers Neuroprotection via Mitochondrial Functional Modulation in a Genetic Parkinson's Disease Model.
Article in CNS neuroscience & therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
backgroundMitochondrial dysfunction is a central pathogenic mechanism in Parkinson's disease (PD), particularly in genetic forms associated with respiratory chain impairment. Disease-modifying therapies capable of restoring neuronal bioenergetics while achieving non-invasive brain delivery remain lacking. This study investigated the therapeutic potential of an arginine-enriched penetratin-derived peptide (PenArg) in a genetic PD model carrying the UQCRC1 (p.Tyr314Ser) mutation.
methodsThe effects of PenArg labeled with 5-FAM- or biotin were evaluated in UQCRC1 knock-in SH-SY5Y cells and mice. Mitochondrial function, neuronal survival, and apoptosis were assessed using biochemical and imaging analyses. Brain distribution was evaluated 2 h after intranasal administration, and therapeutic efficacy was examined following chronic intranasal treatment (three times weekly for six months).
resultsPenArg restored mitochondrial membrane potential, improved neuronal viability, and reduced oxidative stress-induced apoptosis in cellular models. Imaging studies demonstrated partial mitochondrial localization in vitro and in vivo. Intranasal administration significantly improved locomotor performance, preserved dopaminergic neurons in the substantia nigra (SN) and striatum, and maintained hippocampal neuronal structure. Brain distribution analysis confirmed widespread brain penetration after intranasal administration. PenArg restored ATP synthase subunit beta expression and complex III activity while reducing cytochrome c release and caspase-3 activation in SN neurons. Treatment additionally attenuated skeletal muscle atrophy, enhanced antioxidant responses, and reduced circulating pro-inflammatory cytokines.
conclusionPenArg confers neuroprotection through functional modulation of mitochondrial homeostasis and produces multisystem therapeutic benefits. Intranasal administration represents a non-invasive strategy with disease-modifying potential for mitochondrial-related neurodegenerative disorders.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.