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An astrocyte-neuron HSPB1 axis preserves lysosomal integrity and protects from tau pathology
Jimenez-Sanchez M, Lobo PB, Yang F, Power C, Böken D, Verlin L, Guzman-Hernandez R, Cantallops-Jimenez S et al.. Research Square, 2026-10-12
Topic: Disease mechanisms in lab and animal studies
Alzheimer’s disease (AD) is characterized by a decline in neuronal proteostasis that favours the accumulation of misfolded proteins. Molecular chaperones are essential to prevent protein aggregation and, although typically studied as intracellular proteins, chaperones can also be secreted with functions that remain to be elucidated. Here, we identify a mechanism by which astrocyte-secreted HSPB1 is internalized by neurons to increase neuronal proteostasis and prevent the aggregation of pathological tau. We characterized HSPB1 as an astrocytic protein that can also be acquired post-transcriptionally by neurons in AD brain and in culture. Upon internalization into the endolysosomal system through macropinocytosis, HSPB1 prevents lysosomal damage and promotes tau clearance, thereby positioning HSPB1 as a key protein in maintaining organelle and protein homeostasis across astrocyte-neuronal networks. This work identifies a mechanism by which astrocytes boost neuronal capacity to protect from protein aggregation in neurodegeneration.
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APA 7th
Jimenez-Sanchez, M., Lobo, P. B., Yang, F., Power, C., Böken, D., Verlin, L., et al. (2026). An astrocyte-neuron HSPB1 axis preserves lysosomal integrity and protects from tau pathology. Research Square. https://doi.org/10.21203/rs.3.rs-11192311/v1
Vancouver
Jimenez-Sanchez M, Lobo PB, Yang F, Power C, Böken D, Verlin L, et al. An astrocyte-neuron HSPB1 axis preserves lysosomal integrity and protects from tau pathology. Research Square. 2026. doi:10.21203/rs.3.rs-11192311/v1.
BibTeX
@article{jimenezsanchez2026-0a11e557,
author = {Jimenez-Sanchez, M. and Lobo, P. B. and Yang, F. and Power, C. and Böken, D. and Verlin, L. and Guzman-Hernandez, R. and Cantallops-Jimenez, S. and others},
title = {{An astrocyte-neuron HSPB1 axis preserves lysosomal integrity and protects from tau pathology}},
journal = {Research Square},
year = {2026},
doi = {10.21203/rs.3.rs-11192311/v1},
url = {https://doi.org/10.21203/rs.3.rs-11192311/v1}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
Key findings
- Molecular chaperones are essential to prevent protein aggregation and, although typically studied as intracellular proteins, chaperones can also be secreted with functions that remain to be elucidated.
- Here, we identify a mechanism by which astrocyte-secreted HSPB1 is internalized by neurons to increase neuronal proteostasis and prevent the aggregation of pathological tau.
- We characterized HSPB1 as an astrocytic protein that can also be acquired post-transcriptionally by neurons in AD brain and in culture.
- Upon internalization into the endolysosomal system through macropinocytosis, HSPB1 prevents lysosomal damage and promotes tau clearance, thereby positioning HSPB1 as a key protein in maintaining organelle and protein homeostasis across astrocyte-neuronal networks.
- This work identifies a mechanism by which astrocytes boost neuronal capacity to protect from protein aggregation in neurodegeneration.
Study details
- Evidence strengthLow
How this study scored 16/100
Preprint — not yet peer-reviewed. It scored 21 on the same rubric, but non-peer-reviewed sources are capped at 16, so it shows as 16. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 13 of the 62 points we could judge it on, which is 21 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 2 / 10 | Tier 4 — not a peer-reviewed journal (Research Square) |
| Journal's citation record | 0 / 4 | Not a journal article, so the journal's record does not count |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 4 / 10 | Preprint — not yet peer-reviewed. Hosted on a preprint server. |
| How recent | 5 / 5 | 2026 — within 1 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 1 / 2 | Not in PubMed, but has a DOI |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 13 / 62 | Scored on 12 of 20 parts. We have no data for the rest, so they are left out: 13 of the 62 points we could judge it on is 21 out of 100. |
| Total | 21 / 100 | Capped to 16 because this is not a peer-reviewed article. |
What each of these 20 components measures, and what this score is not →
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