2026-07-21T15:21:43Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/97882025-06-13T08:18:50Zcom_20.500.12105_2052com_20.500.12105_2051col_20.500.12105_19617
Repisalud
author
Moreno-García, Alexandra
author
Kun, Alejandra
author
Calero, Olga
author
Medina, Miguel
author
Calero, Miguel
funder
Ministerio de Economía, Industria y Competitividad (España)
funder
Centro de Investigación Biomedica en Red - CIBER
2020-04-28T13:45:45Z
2020-04-28T13:45:45Z
2018
Front Neurosci. 2018 Jul 5;12:464.
10.3389/fnins.2018.00464
1662-4548
Frontiers in neuroscience
30026686
http://hdl.handle.net/20.500.12105/9788
Despite aging being by far the greatest risk factor for highly prevalent neurodegenerative disorders, the molecular underpinnings of age-related brain changes are still not well understood, particularly the transition from normal healthy brain aging to neuropathological aging. Aging is an extremely complex, multifactorial process involving the simultaneous interplay of several processes operating at many levels of the functional organization. The buildup of potentially toxic protein aggregates and their spreading through various brain regions has been identified as a major contributor to these pathologies. One of the most striking morphologic changes in neurons during normal aging is the accumulation of lipofuscin (LF) aggregates, as well as, neuromelanin pigments. LF is an autofluorescent lipopigment formed by lipids, metals and misfolded proteins, which is especially abundant in nerve cells, cardiac muscle cells and skin. Within the Central Nervous System (CNS), LF accumulates as aggregates, delineating a specific senescence pattern in both physiological and pathological states, altering neuronal cytoskeleton and cellular trafficking and metabolism, and being associated with neuronal loss, and glial proliferation and activation. Traditionally, the accumulation of LF in the CNS has been considered a secondary consequence of the aging process, being a mere bystander of the pathological buildup associated with different neurodegenerative disorders. Here, we discuss recent evidence suggesting the possibility that LF aggregates may have an active role in neurodegeneration. We argue that LF is a relevant effector of aging that represents a risk factor or driver for neurodegenerative disorders.
eng
Aging
Amyloid
Autofluorescence
Lipofuscin
Neurodegeneration
Oxidative stress
Protein deposits
An Overview of the Role of Lipofuscin in Age-Related Neurodegeneration
research article
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AnOverviewOfThe_2018.pdf
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AnOverviewOfThe_2018.pdf.txt