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@ARTICLE{Ali:285814,
      author       = {Ali, Mehak and Mehreen, Mehwish and Batool, Saima and Khan,
                      Shahrukh and Noor, Aneeqa and Mumtaz, Sara and Zafar, Saima},
      title        = {{C}hrysoeriol-{M}ediated {N}europrotection in {P}arkinson's
                      {D}isease in {M}ice: {T}argeting {A}poptosis, α-{S}ynuclein
                      {A}ccumulation, and {F}unctional {R}ecovery.},
      journal      = {Yale journal of biology and medicine},
      volume       = {99},
      number       = {1},
      issn         = {0044-0086},
      address      = {New Haven, Conn.},
      publisher    = {[Verlag nicht ermittelbar]},
      reportid     = {DZNE-2026-00350},
      pages        = {111 - 126},
      year         = {2026},
      abstract     = {Parkinson's disease (PD) is a neurodegenerative disorder
                      marked by the progressive loss of dopaminergic neurons in
                      the substantia nigra pars compacta, leading to significant
                      motor dysfunction. Current treatments stabilize dopamine
                      levels but fail to address underlying neuronal apoptosis,
                      highlighting the need for novel approaches. Although
                      chrysoeriol, a 3'-O-methoxy flavone and luteolin derivative,
                      is well-documented for its anti-cancer, anti-diabetic,
                      antioxidant, and anti-inflammatory properties, its
                      neuroprotective potential in PD, particularly in vivo,
                      remains largely unexplored. This study fills a critical gap
                      by being the first to systematically assess chrysoeriol's
                      neuroprotective effects in a PD mouse model. We evaluated
                      the effects of 5 mg/kg chrysoeriol administered
                      intraperitoneally (IP) for 14 days in an acute
                      1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced
                      PD model. Behavioral tests showed notable recovery, as
                      chrysoeriol eliminated deficits in motor function,
                      coordination, and balance, as assessed by the pole test,
                      forced swim test, and tail suspension test. It also
                      mitigated exploratory and locomotor deficits in the open
                      field test, and the Y-maze test revealed improved spatial
                      and learning memory. Hematoxylin and eosin staining
                      indicated a significant reduction in neuronal damage across
                      key brain regions. qPCR analysis showed reduced
                      1-methyl-4-phenylpyridinium (MPP+)-induced toxicity,
                      downregulation of α-synuclein, and an improved Bcl-2/Bax
                      ratio. These findings suggest chrysoeriol may protect
                      against MPP+-induced apoptosis in mice, potentially via the
                      PI3K/Akt signaling pathway, and reduces mitochondrial damage
                      by downregulating α-synuclein.},
      keywords     = {Animals / Apoptosis: drug effects / alpha-Synuclein:
                      metabolism / Neuroprotective Agents: pharmacology /
                      Neuroprotective Agents: therapeutic use / Male / Parkinson
                      Disease: drug therapy / Parkinson Disease: metabolism / Mice
                      / Mice, Inbred C57BL / Disease Models, Animal / Recovery of
                      Function: drug effects / Flavones: pharmacology /
                      Neuroprotection: drug effects / Dopaminergic Neurons: drug
                      effects / Dopaminergic Neurons: metabolism / BAX (Other) /
                      Bcl-2 (Other) / Neuroprotective (Other) / Parkinson’s
                      disease (Other) / chrysoeriol (Other) / α-Synuclein (Other)
                      / alpha-Synuclein (NLM Chemicals) / Neuroprotective Agents
                      (NLM Chemicals) / Flavones (NLM Chemicals)},
      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:41918512},
      pmc          = {pmc:PMC13023422},
      doi          = {10.59249/CTWM1697},
      url          = {https://pub.dzne.de/record/285814},
}