Lysosome activation clears aggregates and enhances quiescent neural stem cell activation during aging
Open accessAbstract
Lysosomes keep neuronal stem cells young: An important consequence of aging is loss of regenerative capacity in stem cells, particularly those of the nervous system. Leeman et al. isolated quiescent and activated stem cells from mice and compared their transcriptomes. The findings emphasize the role of large lysosomes in quiescent neuronal stem cells in which aggregated proteins accumulate. Treatments that stimulated lysosomal function allowed aged quiescent stem cells to clear protein aggregates and restored the cells' ability to be activated. Such restoration of stem cell function might alleviate compromised proteostasis in aging. Science , this issue p. 1277
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In quiescent neural stem cells from old mice, lysosome activity decreases with age and protein aggregates accumulate.
“In quiescent NSCs from old mice, an age-dependent reduction of lysosome activity with accumulated protein aggregates was observed.”
From NAD+ in Brain Aging and Neurodegenerative Disorders (2019) · cites this paper as Leeman et al., 2018
Enhancing lysosome activity in old quiescent neural stem cells by TFEB expression or rapamycin clears protein aggregates and inhibits NSC activation to maintain a youthful state.
“Genetic (expression of the transcription factor EB/TFEB, a master regulator of autophagy and lysosome biogenesis) or pharmacological (feeding with the mTOR inhibitor rapamycin) enhancement of the lysosome activity in old quiescent NSCs cleared protein aggregates and inhibited the NSCs’ activation to maintain the “youthful state” (Leeman et al., 2018).”
From NAD+ in Brain Aging and Neurodegenerative Disorders (2019) · cites this paper as Leeman et al., 2018
Activated NSCs exhibit fewer overall transcriptomic changes with ageing than quiescent NSCs.
“Interestingly, activated NSCs exhibit fewer overall transcriptomic changes with ageing than quiescent NSCs6–9,63,64, perhaps because activated NSCs are recently generated and do not have the time to accumulate damage, or because they ‘dilute’ the damage as they proliferate.”
From Ageing and rejuvenation of tissue stem cells and their niches (2023) · cites this paper as [64]
Age-dependent NSC decline can be reversed by expression of the master transcription factor for lysosomes TFEB and by nutrient deprivation.
“Interestingly, age-dependent NSC decline can be reversed by expression of the master transcription factor for lysosomes TFEB and by nutrient deprivation64.”
From Ageing and rejuvenation of tissue stem cells and their niches (2023) · cites this paper as [64]
Lysosomes are large and abundant in quiescent NSCs.
“For example, lysosomes are large and abundant in quiescent NSCs64.”
From Ageing and rejuvenation of tissue stem cells and their niches (2023) · cites this paper as [64]
Lysosome clearing properties decline with age, resulting in protein aggregate accumulation.
“Lysosome clearing properties decline with age, resulting in protein aggregate accumulation64.”
From Ageing and rejuvenation of tissue stem cells and their niches (2023) · cites this paper as [64]
Inducing the lysosome and autophagy pathways can boost old NSC activation out of quiescence.
“These results suggest that inducing the lysosome and autophagy pathways can boost old NSC activation out of quiescence64.”
From Ageing and rejuvenation of tissue stem cells and their niches (2023) · cites this paper as [64]
Rapamycin treatment in old mice increases the percentage of activated NSCs.
“For example, rapamycin treatment in old mice increases the percentage of activated NSCs64 and rejuvenates HSCs216.”
From Ageing and rejuvenation of tissue stem cells and their niches (2023) · cites this paper as [64]
The previously reported aging-related decline of NRP was confirmed.
“Nonetheless, we were able to confirm the previously reported aging-related decline of certain cell populations, such as NRP 35,36”
From Single-cell transcriptomic profiling of the aging mouse brain (2019) · cites this paper as [36]
The previously reported aging-related decline of OPC, NRP and ImmN was observed.
“Nonetheless, we did observe the previously reported aging-related decline of OPC 49 , NRP 35,36 and ImmN 36,50 .”
From Single-cell transcriptomic profiling of the aging mouse brain (2019) · cites this paper as [36]
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- Authors
- Leeman, D. S., Hebestreit, K., Ruetz, T., Webb, A. E., McKay, A., Pollina, E. A., Dulken, B. W., Zhao, X., Yeo, R. W., Ho, T. T., Mahmoudi, S., Devarajan, K., Passegué, E., Rando, T. A., Frydman, J., & Brunet, A.
- Affiliations
- Stanford University (US)
- University of California, San Francisco (US)
- The Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, Department of Medicine, Division of Hematology and Oncology, University of California, San Francisco, San Francisco, CA 94143, USA.
- Stanford Medicine (US)
- Corresponding author
- Brunet, Anne
- ORCID
- Venue
- Science
- Published
- 2018-03-16
- Volume
- 359
- Issue
- 6381
- Pages
- 1277-1283
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC5915358
- OpenAlex
- W2792158423
- Cited by
- 528
- References
- 49
- Citations by year
- 2026: 35 · 2025: 51 · 2024: 78 · 2023: 72 · 2022: 70 · 2021: 93 · 2020: 64 · 2019: 46 · 2018: 19
- FWCI
- 20.44
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Science Foundation (T32 GM7365 ,P01 AG036695,T32 CA09302)
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- neural stem cells, quiescent neural stem cells, protein aggregates, proteostasis, aging, proteasome, stem cell activation, lysosomal function, brain aging
- MeSH terms
- Aging, Animals, Cell Division, Lysosomes, Mice, Inbred C57BL, Cellular Senescence, Mice, Neural Stem Cells
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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