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Peer-reviewedCC BY 4.0Molecules

Curcumin Prevents Degeneration of Medial Septal Cholinergic Neurons Produced by Parkinsonism-Inducing Neurotoxin 1-Methyl-4-Phenylpyridinium

  • Paola Lenzi1
  • Michela Ferrucci1
  • Gloria Lazzeri1
  • Alessandra Polzella2
  • Marco Scotto3
  • Francesca Biagioni4
  • Paola Binda1
  • Carla L. Busceti4
  • Francesco Fornai1,4
4 affiliations
  1. 1Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, 56126 Pisa, Italy
  2. 2School of Psychology, Sigmund Freud Privat Universität Wien, Milan Campus, 20143 Milan, Italy
  3. 3Department Translational Medicine, Sant’Anna School of Advanced Studies, 56126 Pisa, Italy
  4. 4Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Neuromed, 86077 Pozzilli, Italy
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Abstract

The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine is converted into the active metabolite 1-methyl-4-phenylpyridinium (MPP+), which damages dopamine (DA)-containing neurons of Substantia Nigra, and norepinephrine (NE)-containing neurons of Locus Coeruleus, thus mimicking the pathology of Parkinson’s disease (PD). In PD, cognitive impairment often occurs, which may be due to a loss of acetylcholine (ACh)-containing neurons within the basal forebrain. In turn, this may result from either direct damage to ACh neurons or indirect damage through loss of their DA and/or NE innervation. In the present study, we used neurons from the medial septal nucleus (MSN), which grow in the absence of DA or NE innervation, to assess the direct effects of MPP+ on MSN-derived ACh neurons. Administration of MPP+ directly damages MSN-derived neurons, as evidenced by neuronal loss and dramatic mitochondrial alterations. The phytochemical curcumin administered before MPP+ prevents ACh neuronal damage and mitochondrial derangement. Curcumin administration following MPP+ still promotes neuronal survival while reshaping both damaged mitochondria and cellular processes of ACh neurons. These latter effects are consistent with the expression of key proteins such as PINK1, Parkin, and LC3-II and activation of autophagy flux.

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Cite

BibTeXRIS
BibTeX
@article{lenzi2026curcumin,
  title = {{Curcumin Prevents Degeneration of Medial Septal Cholinergic Neurons Produced by Parkinsonism-Inducing Neurotoxin 1-Methyl-4-Phenylpyridinium}},
  author = {Paola Lenzi and Michela Ferrucci and Gloria Lazzeri and Alessandra Polzella and Marco Scotto and Francesca Biagioni and Paola Binda and Carla L. Busceti and Francesco Fornai},
  journal = {Molecules},
  year = {2026},
  month = oct,
  doi = {10.3390/molecules31213814},
  url = {https://www.mdpi.com/1420-3049/31/21/3814},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Curcumin Prevents Degeneration of Medial Septal Cholinergic Neurons Produced by Parkinsonism-Inducing Neurotoxin 1-Methyl-4-Phenylpyridinium
AU  - Paola Lenzi
AU  - Michela Ferrucci
AU  - Gloria Lazzeri
AU  - Alessandra Polzella
AU  - Marco Scotto
AU  - Francesca Biagioni
AU  - Paola Binda
AU  - Carla L. Busceti
AU  - Francesco Fornai
PY  - 2026
DA  - 2026/10/22
JO  - Molecules
DO  - 10.3390/molecules31213814
UR  - https://www.mdpi.com/1420-3049/31/21/3814
AB  - The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine is converted into the active metabolite 1-methyl-4-phenylpyridinium (MPP+), which damages dopamine (DA)-containing neurons of Substantia Nigra, and norepinephrine (NE)-containing neurons of Locus Coeruleus, thus mimicking the pathology of Parkinson’s disease (PD). In PD, cognitive impairment often occurs, which may be due to a loss of acetylcholine (ACh)-containing neurons within the basal forebrain. In turn, this may result from either direct damage to ACh neurons or indirect damage through loss of their DA and/or NE innervation. In the present study, we used neurons from the medial septal nucleus (MSN), which grow in the absence of DA or NE innervation, to assess the direct effects of MPP+ on MSN-derived ACh neurons. Administration of MPP+ directly damages MSN-derived neurons, as evidenced by neuronal loss and dramatic mitochondrial alterations. The phytochemical curcumin administered before MPP+ prevents ACh neuronal damage and mitochondrial derangement. Curcumin administration following MPP+ still promotes neuronal survival while reshaping both damaged mitochondria and cellular processes of ACh neurons. These latter effects are consistent with the expression of key proteins such as PINK1, Parkin, and LC3-II and activation of autophagy flux.
SN  - 1420-3049
ER  -