When longevity becomes chemistry: Why rodent brains lack neuromelanin
- 1CNS Gene Therapy Program, Center for Applied Medical Research (CIMA), University of Navarra, Pamplona, Spain
Abstract
Background: The biology of neuromelanin (NMel) is linked to Parkinson's disease, in which pigment accumulation and release contribute to dopaminergic cell loss. Rodent brains lack detectable levels of NMel, despite possessing the molecular machinery required for its synthesis. The basis for this absence remains unknown. Objectives: To determine whether long-living rodents accumulate NMel and to test whether lifespan constraints explain the lack of pigmentation in mice and rats. Methods: Histological stains were conducted in brain samples of mole rats of different ages to disclose the potential pigmentation of catecholaminergic centers and to determine the chemical phenotype of pigmented neurons. Results: Mole rats exhibited clear age-dependent NMel accumulation beginning after two years of age, with the highest pigmentation levels observed in neurons of the locus coeruleus. Conclusions: Accumulation of NMel is a slow kinetic process that requires extended longevity. Common laboratory rodents lack pigmented brains simply because they do not live long enough to reach detectable NMel levels.
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BibTeX
@misc{canales2026when,
title = {{When longevity becomes chemistry: Why rodent brains lack neuromelanin}},
author = {C. Canales and M. M. Ilarduya and J. Chocarro and A. J. Rico and G. Gariznabarreta and E. Lorenzo-Ramos and D. Carbonell and R. Sumbera and J. Okrouhlik and D. Ruiz-Molina and J. L. Lanciego},
howpublished = {bioRxiv},
year = {2026},
month = oct,
doi = {10.64898/2026.10.13.759023},
url = {https://www.biorxiv.org/content/10.64898/2026.10.13.759023v1},
note = {CC BY},
}
RIS
TY - UNPB
TI - When longevity becomes chemistry: Why rodent brains lack neuromelanin
AU - C. Canales
AU - M. M. Ilarduya
AU - J. Chocarro
AU - A. J. Rico
AU - G. Gariznabarreta
AU - E. Lorenzo-Ramos
AU - D. Carbonell
AU - R. Sumbera
AU - J. Okrouhlik
AU - D. Ruiz-Molina
AU - J. L. Lanciego
PY - 2026
DA - 2026/10/13
PB - bioRxiv
DO - 10.64898/2026.10.13.759023
UR - https://www.biorxiv.org/content/10.64898/2026.10.13.759023v1
AB - Background: The biology of neuromelanin (NMel) is linked to Parkinson's disease, in which pigment accumulation and release contribute to dopaminergic cell loss. Rodent brains lack detectable levels of NMel, despite possessing the molecular machinery required for its synthesis. The basis for this absence remains unknown. Objectives: To determine whether long-living rodents accumulate NMel and to test whether lifespan constraints explain the lack of pigmentation in mice and rats. Methods: Histological stains were conducted in brain samples of mole rats of different ages to disclose the potential pigmentation of catecholaminergic centers and to determine the chemical phenotype of pigmented neurons. Results: Mole rats exhibited clear age-dependent NMel accumulation beginning after two years of age, with the highest pigmentation levels observed in neurons of the locus coeruleus. Conclusions: Accumulation of NMel is a slow kinetic process that requires extended longevity. Common laboratory rodents lack pigmented brains simply because they do not live long enough to reach detectable NMel levels.
ER -