ArticleStem cell research & therapy2026
Adcyap1r1-driven astrocyte reprogramming attenuates neuroinflammation and promotes dopaminergic neuroprotection in Parkinson's Disease.
Article in Stem cell research & therapy, 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
backgroundParkinson's disease (PD), the second most prevalent neurodegenerative disorder globally, is characterized by progressive degeneration of dopaminergic (DA) neurons and sustained neuroinflammatory cascades. Strategies that simultaneously suppress neuroinflammation and protect DA neurons are urgently needed, particularly through targeting astrocytes (As). Building on our previous discovery that combined miR-124 and small molecule interventions synergistically suppress As activation and induce their transdifferentiation into dopaminergic-like neurons, this study identified Adcyap1r1 as a pivotal regulator via RNA-seq analysis. Here, we systematically investigated its cAMP-mediated dual functional roles in neuroinflammatory modulation and DA neuron preservation.
methodsTGF-β1-activated neonatal SD rat cortical reactive astrocytes (RAs) were used for Adcyap1r1 overexpression. We assessed astrocyte reactivity, neuroinflammation, neuron-like transition, and cAMP pathway activity in vitro. In MPTP-induced PD mice, AAV-mediated Adcyap1r1 overexpression was targeted to striatal As. Motor function, astrocyte activation, neuroinflammation, and endogenous DA neuron survival in the nigrostriatal system were evaluated through behavioral, histopathological, and molecular analyses.
resultsIn activated RAs, Adcyap1r1 overexpression significantly attenuated reactivity, reduced pro-inflammatory mediator expression (e.g., COX-2, iNOS), activated cAMP signaling, and promoted the acquisition of a tyrosine hydroxylase-positive (TH
conclusionsOur study demonstrates that Adcyap1r1 functions through a cAMP-dependent dual mechanism to suppress astrocyte reactivity and neuroinflammatory cascades, and facilitate the transition of RAs into a DA neuron-like phenotype. This dual regulatory mechanism protects the nigrostriatal DA system and ameliorates motor dysfunction in PD mice, providing a theoretical foundation for developing innovative therapeutic strategies against PD.
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.