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27/100

✓ Peer-reviewed alzhub usefulness score 27 out of 100. Disease mechanisms

Topic: Amyloid, tau and blood-test diagnosis

Plain-language summary

Alzheimer’s disease is the leading cause of dementia and represents a growing global health challenge. The disease is neuropathologically defined by extracellular amyloid beta deposits and intracellular neurofibrillary tangles composed of hyperphosphorylated tau protein. However, decades of research demonstrate that these hallmarks alone cannot fully account for the clinical and biological complexity of Alzheimer’s disease. Advanced glycation end-products, formed through non-enzymatic glycation and oxidation of proteins, lipids, and nucleic acids, have emerged as key contributors to neurodegeneration. Advanced glycation end-products accumulate progressively with age, and their formation is intensified by hyperglycaemia and oxidative stress. Their presence has been demonstrated in both senile plaques and neurofibrillary tangles. By irreversibly modifying long-lived proteins, advanced glycation end-products alter their structural and enzymatic properties, promote amyloid aggregation, and predispose tau to hyperphosphorylation. Importantly, their interaction with the receptor for advanced glycation end-products initiates signalling cascades that amplify oxidative stress, inflammation, mitochondrial dysfunction, and synaptic impairment. Beyond their direct neuronal effects, advanced glycation end-products link Alzheimer’s disease with systemic comorbidities such as diabetes, vascular disease, and chronic kidney disease, all of which further increase dementia risk. Clinical studies report elevated levels of advanced glycation end-products in serum, cerebrospinal fluid, and brain tissue of Alzheimer’s disease patients, suggesting their utility as potential biomarkers. Therapeutic strategies, including advanced glycation end-products inhibitors, cross-link breakers, receptor for advanced glycation end-products antagonists, antioxidant compounds, and dietary interventions, are currently under investigation, although their clinical efficacy remains limited. This review highlights the multifaceted role of advanced glycation end-products in the pathogenesis of Alzheimer’s disease, underscores their clinical relevance, and points to future research directions in diagnosis, prevention, and treatment.

What this study adds

Evidence grade: Low

This review describes how advanced glycation end-products accumulate with age and are found in senile plaques and neurofibrillary tangles, where they can promote amyloid aggregation and tau hyperphosphorylation. It is a review of mechanisms only and does not report any treatment, cure, or prevention tested in patients.

Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.

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

APA 7th

Mazur, K., & Smoleń, A. (2026). Advanced glycation end-products in the pathogenesis of Alzheimer’s disease: a review. Psychiatria i Psychologia Kliniczna. https://doi.org/10.15557/pipk.2026.0011

Vancouver

Mazur K, Smoleń A. Advanced glycation end-products in the pathogenesis of Alzheimer’s disease: a review. Psychiatria i Psychologia Kliniczna. 2026. doi:10.15557/pipk.2026.0011.

BibTeX

@article{mazur2026-52694e77,
  author  = {Mazur, Karol and Smoleń, Agata},
  title   = {{Advanced glycation end-products in the pathogenesis of Alzheimer’s disease: a review}},
  journal = {Psychiatria i Psychologia Kliniczna},
  year    = {2026},
  doi     = {10.15557/pipk.2026.0011},
  url     = {https://doi.org/10.15557/pipk.2026.0011}
}

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How to read this study

Design: our record does not state a study design, so check the methods section of the original before weighing the result.
Size: the record gives no participant count. Look for one in the original before trusting a pattern.
Effect: the record gives no effect size, so the summary above cannot say how large any difference was.

What the evidence grade means here

This page is graded low. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Low means the abstract matched neither pattern. It is the default label, and it does not mean the work is poor; many sound lab and imaging papers land here. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

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Key findings

Their presence has been demonstrated in both senile plaques and neurofibrillary tangles.

Why it matters

Study details

Evidence strengthLow

How this study scored 27/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Psychiatria i Psychologia Kliniczna)
Journal's citation record	0 / 4	Psychiatria i Psychologia Kliniczna: journal h-index 15 (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	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)
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	0 / 7	Cited 0 times (OpenAlex, 2026-10-10)
Citations per year	0 / 5	0.0 citations a year over 2 year(s) since 2026
Impact for its field and year	0 / 6	Cited 0.0× 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	0 / 4	Cited 0 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	1 / 4	Last-listed author Agata Smoleń: h-index 18 (OpenAlex, whole career)
Institution's track record	0 / 3	Medical University of Lublin: institution h-index 295 (OpenAlex)
Multicenter collaboration	0 / 3	OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete)
Indexed in PubMed	1 / 2	Not in PubMed, but has a DOI
Free to read	2 / 2	Free to read
Total	27 / 100	—

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

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