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@ARTICLE{Mehreen:277980,
      author       = {Mehreen, Mehwish and Ali, Mehak and Tariq, Huraira and
                      Noor, Aneeqa and Mumtaz, Sara and Zafar, Saima},
      title        = {{C}henodeoxycholic {A}cid-{M}ediated neuroprotection via
                      α-synuclein and {BDNF} {M}odulation in {MPTP}-{I}nduced
                      mouse model of {P}arkinson's disease.},
      journal      = {Neuroscience},
      volume       = {573},
      issn         = {0306-4522},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {DZNE-2025-00512},
      pages        = {442 - 450},
      year         = {2025},
      abstract     = {Parkinson's disease (PD) remains a major challenge in the
                      field of neurodegenerative diseases and requires innovative
                      therapeutic approaches. In this study, we investigated the
                      therapeutic potential of chenodeoxycholic acid (CDCA) in PD
                      using a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine
                      (MPTP)-induced mouse model. CDCA, a naturally occurring bile
                      acid, has previously shown promise in various neurological
                      disorders by reducing neuronal degeneration and promoting
                      neuronal health, however its utility in PD has not been
                      studied. We divided mice into a control group, an
                      MPTP-induced PD model and a treatment group injected with
                      CDCA. CDCA reduced motor impairment and ameliorated
                      anxiety-like behavior as assessed through the pole and open
                      field test, demonstrated antidepressant effects in the
                      forced swim and tail suspension test, and results of the
                      Y-maze test showed improved cognitive performance.
                      Furthermore, the effective defense against MPTP-induced
                      dopaminergic degeneration was provided by CDCA by improving
                      the morphological and histological features of neurons in
                      the midbrain, hippocampus, cortex and cerebellum. Analysis
                      via RT-PCR revealed that CDCA significantly mitigated MPP +
                      -induced elevations in α-synuclein levels, indicating its
                      potential to preserve neuronal function by modulating
                      synaptic integrity. Additionally, CDCA effectively reduced
                      the associated toxicity by enhancing the low levels of
                      brain-derived neurotrophic factor. Conclusively, given the
                      increasing prevalence of PD and the urgent need for
                      effective neuroprotective strategies, our findings suggest
                      that CDCA exerts neuroprotective effects in an MPTP-induced
                      PD model. These results highlight CDCA as a promising
                      candidate for further investigation in PD therapy and
                      provide a basis for further research into bile acid-based
                      treatments in neurodegenerative diseases.},
      keywords     = {BDNF (Other) / Chenodeoxycholic acid (Other) / MPTP (Other)
                      / Parkinson’s disease (Other) / α-synuclein (Other)},
      cin          = {AG Zerr},
      ddc          = {610},
      cid          = {I:(DE-2719)1440011-1},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40185387},
      doi          = {10.1016/j.neuroscience.2025.03.050},
      url          = {https://pub.dzne.de/record/277980},
}