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This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Disease mechanisms

Topic: Amyloid, tau and blood-test diagnosis

Neurodegenerative diseases are currently among the most devastating diseases with no effective disease-modifying drugs in the market, with Alzheimer's disease (AD) being the most prevalent. AD is a complex multifactorial neurodegenerative disorder characterized by progressive and severe cognitive impairment and memory loss. It is the most common cause of progressive memory loss (dementia) in the elderly, and to date, there is no effective treatment to cure or slow disease progression substantially. The role of adrenergic receptors in the pathogenesis of Alzheimer's disease and other tauopathies is poorly understood or investigated. Recently, some studies indicated a potential benefit of drugs acting on the adrenergic receptors for AD and dementias, although due to the heterogeneity of the drug classes used, the results on the whole remain inconclusive. The scope of this review article is to comprehensively review the literature on the possible role of adrenergic receptors in neurodegenerative diseases, stemming from the use of agonists and antagonists including antihypertensive and asthma drugs acting on the adrenergic receptors, but also from animal models and in vitro models where these receptors have been studied. Ultimately, we hope to obtain a better understanding of the role of these receptors, identify the gaps in knowledge, and explore the possibility of repurposing such drugs for AD, given their long history of use and safety.

Key findings

Why it matters

This review examines whether drugs acting on adrenergic receptors might benefit Alzheimer's disease and other dementias. It states that results so far remain inconclusive because of the heterogeneity of the drug classes studied, so no treatment or prevention benefit is established.

Study details

How this study scored 38/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 2 of 4; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 4 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomised / blinded 0 of 2; Times cited 2 of 7; Citations per year 2 of 5; Impact for its field and year 3 of 6; Cited by studies here 0 of 6; Still being cited 1 of 4; Senior author's track record 2 of 4; Institution's track record 0 of 3; Multi-centre collaboration 0 of 3; Indexed in PubMed 2 of 2; Free to read 2 of 2. Total 38 of 100.38 of 100 points earned62 not earned

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.

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (Biomolecules)
Journal's citation record 2 / 4 Biomolecules: journal h-index 191 (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 4 / 5 2025 — within 3 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 2 / 7 Cited 13 times (OpenAlex, 2026-10-10)
Citations per year 2 / 5 4.3 citations a year over 3 year(s) since 2025
Impact for its field and year 3 / 6 Cited 7.1× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 0 / 6 No other study in this library cites it
Still being cited 1 / 4 Cited 13 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 2 / 4 Last-listed author Lefteris C. Zacharia: h-index 30 (OpenAlex, whole career)
Institution's track record 0 / 3 University of Nicosia: institution h-index 153 (OpenAlex)
Multi-centre collaboration 0 / 3 OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete)
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 39858522)
Free to read 2 / 2 Free to read
Total 38 / 100 —

What each of these 20 components measures, and what this score is not →

Read the original

Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.

APA 7th

Miliotou, Α. N., Kotsoni, A., & Zacharia, L. C. (2025). Deciphering the Role of Adrenergic Receptors in Alzheimer’s Disease: Paving the Way for Innovative Therapies. Biomolecules. https://doi.org/10.3390/biom15010128

Vancouver

Miliotou ΑN, Kotsoni A, Zacharia LC. Deciphering the Role of Adrenergic Receptors in Alzheimer’s Disease: Paving the Way for Innovative Therapies. Biomolecules. 2025. doi:10.3390/biom15010128. PMID: 39858522.

BibTeX

@article{miliotou2025-39858522,
  author  = {Miliotou, Αndroulla N. and Kotsoni, Andria and Zacharia, Lefteris C.},
  title   = {{Deciphering the Role of Adrenergic Receptors in Alzheimer’s Disease: Paving the Way for Innovative Therapies}},
  journal = {Biomolecules},
  year    = {2025},
  doi     = {10.3390/biom15010128},
  pmid    = {39858522},
  url     = {https://doi.org/10.3390/biom15010128}
}

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