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How Can Hearing Loss Cause Dementia?
Griffiths TD, Lad M, Kumar S, Holmes E, McMurray B, Maguire EA, Billig AJ, Sedley W.. Neuron, 2020-08-31
Topic: Risk, prevention and care in population studies
Epidemiological studies identify midlife hearing loss as an independent risk factor for dementia, estimated to account for 9% of cases. We evaluate candidate brain bases for this relationship. These bases include a common pathology affecting the ascending auditory pathway and multimodal cortex, depletion of cognitive reserve due to an impoverished listening environment, and the occupation of cognitive resources when listening in difficult conditions. We also put forward an alternate mechanism, drawing on new insights into the role of the medial temporal lobe in auditory cognition. In particular, we consider how aberrant activity in the service of auditory pattern analysis, working memory, and object processing may interact with dementia pathology in people with hearing loss. We highlight how the effect of hearing interventions on dementia depends on the specific mechanism and suggest avenues for work at the molecular, neuronal, and systems levels to pin this down.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Griffiths, T. D., Lad, M., Kumar, S., Holmes, E., McMurray, B., Maguire, E. A., et al. (2020). How Can Hearing Loss Cause Dementia? Neuron. https://doi.org/10.1016/j.neuron.2020.08.003
Vancouver
Griffiths TD, Lad M, Kumar S, Holmes E, McMurray B, Maguire EA, et al. How Can Hearing Loss Cause Dementia? Neuron. 2020. doi:10.1016/j.neuron.2020.08.003. PMID: 32871106.
BibTeX
@article{griffiths2020-32871106,
author = {Griffiths, T. D. and Lad, M. and Kumar, S. and Holmes, E. and McMurray, B. and Maguire, E. A. and Billig, A. J. and Sedley, W.},
title = {{How Can Hearing Loss Cause Dementia?}},
journal = {Neuron},
year = {2020},
doi = {10.1016/j.neuron.2020.08.003},
pmid = {32871106},
url = {https://doi.org/10.1016/j.neuron.2020.08.003}
}
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 names 8 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
Key findings
- We evaluate candidate brain bases for this relationship.
- These bases include a common pathology affecting the ascending auditory pathway and multimodal cortex, depletion of cognitive reserve due to an impoverished listening environment, and the occupation of cognitive resources when listening in difficult conditions.
- We also put forward an alternate mechanism, drawing on new insights into the role of the medial temporal lobe in auditory cognition.
- In particular, we consider how aberrant activity in the service of auditory pattern analysis, working memory, and object processing may interact with dementia pathology in people with hearing loss.
- We highlight how the effect of hearing interventions on dementia depends on the specific mechanism and suggest avenues for work at the molecular, neuronal, and systems levels to pin this down.
Why it matters
This paper evaluates several possible brain mechanisms that could explain why midlife hearing loss is linked to dementia, including effects on the auditory pathway, cognitive reserve, and the medial temporal lobe. It suggests that whether hearing interventions reduce dementia risk depends on which mechanism is at work, and calls for further research to clarify this.
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Study details
- Evidence strengthLow
How this study scored 56/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neuron) |
| Journal's citation record | 4 / 4 | Neuron: journal h-index 689 (OpenAlex, 2026-10-29) |
| 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 | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 2 / 5 | 2020 — within 10 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 | 6 / 7 | Cited 372 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 46.5 citations a year over 8 year(s) since 2020 |
| Impact for its field and year | 5 / 6 | Cited 20.8× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 19 other studies in this library |
| Still being cited | 4 / 4 | Cited 204 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author William Sedley: h-index 25 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University College London: institution h-index 2,029 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 6 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 32871106) |
| Free to read | 2 / 2 | Free to read |
| Total | 56 / 100 | — |
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