ReviewFrontiers in neuroscience2018
An Overview of the Role of Lipofuscin in Age-Related Neurodegeneration.
Review in Frontiers in neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 214 papers.
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Who cites it
214 citing papers in PubMed, 388 citations in OpenAlex.
- Progranulin AAV gene therapy for frontotemporal dementia: translational studies and phase 1/2 trial interim results.Nature medicine · 2024Trial
- Insights into the modulation of age-related macular degeneration: Molecular and systems-level perspectives.Acta ophthalmologica · 2026Article
- Spatial proteomic analysis in human Alzheimer's disease brains enables identification of microenvironment-dependent microglial cell states.Nature neuroscience · 2026Article
- Traumatic life experiences during critical periods lead to diverse developmental trajectories.Cell reports. Medicine · 2026Article
- From epigenetic scripts to kinase signals: linking DOT1L and RIPK1 in the neurobiology of degeneration.Molecular biology reports · 2026Review
- Morphological characteristics of corneal stromal stem cells and their age-related decline.Scientific reports · 2026Article
- Lipofuscin accumulation in aging and CLN1 is associated with deficient de-S-acylation, lyso-mitochondrial dysfunction, and lipid dyshomeostasis.Acta neuropathologica · 2026Article
- Lipofuscin: The Missing Link in the Worsening of Obstructive Sleep Apnea.The Laryngoscope · 2026Article
- Type-1 interferons associated with microglial-mediated neuroinflammation in Alzheimer's disease.Journal of neuroinflammation · 2026Review
- activeDISCO enables large-scale exploration of human brain anatomy by light sheet microscopy.Communications biology · 2026Article
- A Novel Central-Peripheral Interface: The Auditory Nerve Glial Transition Zone Exhibits Enhanced Age-Related Immune and Glial Cell Dysfunction.bioRxiv : the preprint server for biology · 2026Article
- Deficient de-S-acylation in aging and CLN1 contributes to lyso-mitochondrial dysfunction, lipid dyshomeostasis, and resultant lipofuscin biogenesis.Research square · 2026Article
- A Pathophysiological Model of Parkinson's Disease Based on Microvascular Flow Disturbance and Leukocyte-Mediated Oxidative Injury in Critical Pigmented Neuronal Niches.Antioxidants (Basel, Switzerland) · 2026Article
- Mitochondria and Lipid Defects in Hereditary Progranulin-Related Frontotemporal Dementia.Cells · 2026Article
- Article
- Discovery of NIRF theranostic probes targeting amyloid-β and cholinesterases in Alzheimer's disease models.Nature communications · 2026Article
- Public concerns over presumed metal and radionuclide pollution: testing a possible link to ovine hepatic melanosis in South Greenland.Environmental monitoring and assessment · 2026Article
- Dysfunction of lipid metabolism and lysosomal capacity: at the core of microglial aging?Frontiers in aging neuroscience · 2026Review
- The auditory nerve glial transition zone is a focal site of age-related immune-myelin interactions.Frontiers in immunology · 2026Article
- The Neurogenic Niche: Interactions Among Vessels, Glia, and Neural Stem Cells.Stem cells international · 2026Review
154 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.