Thioredoxin-1 in the SNpc Regulates Subventricular Zone Neural Proliferation and Olfactory Bulb Neural Differentiation in MPTP-Induced Olfactory Dysfunction.

Xianwen Zhang, Yafang Li, Xiongjie He, Ai Yang, Yali Chen, Fang Yan, Liping Bai, Jie Bai

Abstract read

In one paragraph

Article in Neurochemical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it

0cells of the map it votes in

0citing papers in PubMed

–field-weighted citation impact

1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Xianwen Zhang *Laboratory of Molecular Neurobiology, Medical School, Kunming University of Science and Technology, Kunming, 650500, China.

Yafang Li *Laboratory of Molecular Neurobiology, Medical School, Kunming University of Science and Technology, Kunming, 650500, China.

Xiongjie HeLaboratory of Molecular Neurobiology, Medical School, Kunming University of Science and Technology, Kunming, 650500, China.

Ai YangLaboratory of Molecular Neurobiology, Medical School, Kunming University of Science and Technology, Kunming, 650500, China.

Yali ChenLaboratory of Molecular Neurobiology, Medical School, Kunming University of Science and Technology, Kunming, 650500, China.

Fang YanLaboratory of Molecular Neurobiology, Medical School, Kunming University of Science and Technology, Kunming, 650500, China.

Liping BaiLaboratory of Molecular Neurobiology, Medical School, Kunming University of Science and Technology, Kunming, 650500, China.

Jie BaiLaboratory of Molecular Neurobiology, Medical School, Kunming University of Science and Technology, Kunming, 650500, China. jiebai662001@126.com.ORCID https://orcid.org/0000-0003-1281-3159

Funding

Scientific and Technological Projects of Yunnan Provincial Science and Technology Department 202401AU070130the National Natural Science Foundation of China 81901118the National Natural Science Foundation of China 82371271

6 · The paper itself

Abstract

Despite hyposmia being a dominant non-motor manifestation of Parkinson's disease (PD), its underlying driving mechanisms are poorly defined. The redox protein Thioredoxin-1 (Trx-1) offers neuroprotection against various insults; however, its potential involvement in the neural proliferation in the subventricular zone (SVZ) and neural differentiation in the olfactory bulb (OB) related to MPTP-induced olfactory dysfunction have not been previously established. Our research demonstrates that when Trx-1 is downregulated in the substantia nigra pars compacta (SNpc), MPTP-triggered olfactory deficits are significantly intensified. A key anatomical discovery in our study is the existence of projections from the SNpc to the SVZ. We established that the MPTP-driven death of SNpc dopaminergic (DAergic) neurons correlates with decreased dopamine D1 receptor (D1R) levels in the SVZ, an effect that is magnified by the loss of Trx-1. Alongside D1R reductions, MPTP suppressed a cascade of SVZ signaling molecules (phosphorylated PKA, Wnt3a, β-catenin, Pax6, cyclin D1, and CDK4), with Trx-1 deficiency causing even steeper declines. Furthermore, Trx-1 knockdown hindered the generation of immature neurons and disrupted DAergic neuronal differentiation within the OB. Collectively, our findings suggest that reduced Trx-1 expression in the SNpc may contribute to PD-related olfactory deficits, potentially via inhibiting SVZ neural proliferation, decreasing immature and mature neuron populations, and disrupted differentiation of OB immature neurons. By accelerating MPTP-triggered degeneration of DAergic neurons in the SNpc, Trx-1 downregulation reduces the SVZ of DAergic input. This disruption impairs D1R-mediated the neural proliferation in the SVZ, as well as the maturation and differentiation of immature neurons in OB, ultimately driving the progression of olfactory dysfunction in a PD mouse model.

Indexed as

Cell DifferentiationCell ProliferationLateral VentriclesOlfactory BulbPars CompactaThioredoxinsAnimalsDopaminergic NeuronsMaleMiceMice, Inbred C57BLNeurogenesisThioredoxinsTxn1 protein, mouseOlfactory functionParkinson’s diseaseProliferation and differentiationSubventricular zoneThioredoxin-1

Identifiers

PMID42541661

DOI10.1007/s11064-026-04850-3

What OpenQuestion holds

Textmetadata

Read underepoch 390

Registered trials

None linked

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 OpenQuestion graph.