You say lipofuscin, we say ceroid: Defining autofluorescent storage material
Abstract
Accumulation of intracellular autofluorescent material or "aging pigment" has been characterized as a normal aging event. Certain diseases also exhibit a similar accumulation of intracellular autofluorescent material. However, autofluorescent storage material associated with aging and disease has distinct characteristics. Lipofuscin is a common term for aging pigments, whereas ceroid is used to describe pathologically derived storage material, for example, in the neuronal ceroid lipofuscinoses (NCLs). NCLs are a family of neurodegenerative diseases that are characterized by an accumulation of autofluorescent storage material (ceroid) in the lysosome, which has been termed "lipofuscin-like". There have been many studies that describe this autofluorescent storage material, but what is it? Is this accumulation lipofuscin or ceroid? In this review we will try to answer the following questions: (1) What is lipofuscin and ceroid? (2) What contributes to the accumulation of this storage material in one or the other? (3) Does this material have an effect on cellular function? Studying parallels between the accumulation of lipofuscin and ceroid may provide insight into the biological relevance of these phenomena.
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Lipofuscin is a pathological autofluorescent lipopigment that relates to neuronal aging and vulnerability in AD brain.
“a pathological autofluorescent lipopigment of obscure origin since its discovery in 1840 (reviewed in ref.43) that relates to neuronal aging35,43 and vulnerability in AD brain44”
From Decreased lipidated ApoE‐receptor interactions confer protection against pathogenicity of ApoE and its lipid cargoes in lysosomes (2025) · cites this paper as [43]
When ApoE carries PUFA-CE, LDLR-dependent internalization caused lysosomal deposition of lipofuscin.
“Specifically, when ApoE carries PUFA-CE, LDLR-dependent internalization caused lysosomal deposition of lipofuscin, a pathological autofluorescent lipopigment of obscure origin since its discovery in 1840 (reviewed in ref.43) that relates to neuronal aging35,43 and vulnerability in AD brain44.”
From Decreased lipidated ApoE‐receptor interactions confer protection against pathogenicity of ApoE and its lipid cargoes in lysosomes (2025) · cites this paper as [43]
Lipofuscin arises from oxidative damage and crosslinking of macromolecules induced by PUFA peroxidation.
“Lipofuscin is believed to arise from oxidative damage and crosslinking of macromolecules induced by PUFA peroxidation35,43.”
From Decreased lipidated ApoE‐receptor interactions confer protection against pathogenicity of ApoE and its lipid cargoes in lysosomes (2025) · cites this paper as [43]
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“…when ApoE carries PUFA-CE, LDLR-dependent internalization caused lysosomal deposition of lipofuscin, a pathological autofluores-cent lipopigment of obscure origin since its discovery in 1840 (reviewed in Seehafer and Pearce 43 ) that relates to neuronal aging 35,43 and vulnerability in AD brain.”
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- Authors
- Seehafer, S. S., & Pearce, D. A.
- Affiliations
- University of Rochester Medicine (US)
- Corresponding author
- Pearce, David A
- ORCID
- Pearce, David A
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2006-04
- Volume
- 27
- Issue
- 4
- Pages
- 576-588
- ISSN
- 0197-4580 (ISSN-L)
- OpenAlex
- W2078157157
- Cited by
- 212
- References
- 3
- Citations by year
- 2026: 6 · 2025: 13 · 2024: 11 · 2023: 8 · 2022: 5 · 2021: 12 · 2020: 16 · 2019: 10 · 2018: 9 · 2017: 13 · 2016: 4 · 2015: 12 · 2014: 8 · 2013: 14 · 2012: 11
- FWCI
- 1.47
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (NS036610, NS044310)
- Topics
- Health Sciences › Medicine › Physiology › Lysosomal Storage Disorders Research
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Rheumatology › Glycogen Storage Diseases and Myoclonus
- Keywords
- lipofuscin, ceroid, neuronal ceroid lipofuscinosis, lysosomal storage, neurodegenerative diseases, cellular aging, lysosomes
- MeSH terms
- Aging, Animals, Autophagy, Ceroid, Humans, Lipofuscin, Lysosomes, Models, Biological, Nervous System Diseases, Neuronal Ceroid-Lipofuscinoses, Oxidation-Reduction
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