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50/100

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Inflammation and the immune system

Topic: Amyloid, tau and blood-test diagnosis

Plain-language summary

Alzheimer's disease (AD) is the most common cause of progressive dementia in the elderly. It is characterized by a progressive and irreversible loss of cognitive abilities and formation of senile plaques, composed mainly of amyloid β (Aβ), and neurofibrillary tangles (NFTs), composed of tau protein, in the hippocampus and cortex of afflicted humans. In brains of AD patients the metabolism of Aβ is dysregulated, which leads to the accumulation and aggregation of Aβ.

What this study adds

Evidence grade: Low

This is a narrative review. This review states that the metabolism of amyloid-beta and tau is influenced by autophagy, a lysosome-dependent process, and discusses therapeutic implications. It reports no treatment, cure or prevention that has been established.

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

Uddin, M. S., Stachowiak, A., Mamun, A. A., Tzvetkov, N. T., Takeda, S., Atanasov, A. G., et al. (2018). Autophagy and Alzheimer's Disease: From Molecular Mechanisms to Therapeutic Implications. Frontiers in aging neuroscience. https://doi.org/10.3389/fnagi.2018.00004

Vancouver

Uddin MS, Stachowiak A, Mamun AA, Tzvetkov NT, Takeda S, Atanasov AG, et al. Autophagy and Alzheimer's Disease: From Molecular Mechanisms to Therapeutic Implications. Frontiers in aging neuroscience. 2018. doi:10.3389/fnagi.2018.00004. PMID: 29441009.

BibTeX

@article{uddin2018-29441009,
  author  = {Uddin, M. S. and Stachowiak, A. and Mamun, A. A. and Tzvetkov, N. T. and Takeda, S. and Atanasov, A. G. and Bergantin, L. B. and Abdel-Daim, M. M. and others},
  title   = {{Autophagy and Alzheimer's Disease: From Molecular Mechanisms to Therapeutic Implications}},
  journal = {Frontiers in aging neuroscience},
  year    = {2018},
  doi     = {10.3389/fnagi.2018.00004},
  pmid    = {29441009},
  url     = {https://doi.org/10.3389/fnagi.2018.00004}
}

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.

How to read this study

Design: this is a narrative review. It summarises a field without a fixed search method, so it shows how authors read the evidence rather than measuring it. Use it to find the primary studies, not as a result in itself.
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

It is characterized by a progressive and irreversible loss of cognitive abilities and formation of senile plaques, composed mainly of amyloid β (Aβ), and neurofibrillary tangles (NFTs), composed of tau protein, in the hippocampus and cortex of afflicted humans.
In brains of AD patients the metabolism of Aβ is dysregulated, which leads to the accumulation and aggregation of Aβ.
Metabolism of Aβ and tau proteins is crucially influenced by autophagy.
Autophagy is a lysosome-dependent, homeostatic process, in which organelles and proteins are degraded and recycled into energy.

Why it matters

This review states that the metabolism of amyloid-beta and tau is influenced by autophagy, a lysosome-dependent process, and discusses therapeutic implications. It reports no treatment, cure or prevention that has been established.

Study details

Evidence strengthLow

How this study scored 50/100

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 (Frontiers in aging neuroscience)
Journal's citation record	2 / 4	Frontiers in Aging Neuroscience: journal h-index 174 (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	2018 — 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)
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	6 / 7	Cited 441 times (OpenAlex, 2026-10-10)
Citations per year	4 / 5	44.1 citations a year over 10 year(s) since 2018
Impact for its field and year	5 / 6	Cited 29.2× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	2 / 6	Cited by 9 other studies in this library
Still being cited	3 / 4	Cited 146 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	1 / 4	Last-listed author Adrian Mateusz Stankiewicz: h-index 15 (OpenAlex, whole career)
Institution's track record	1 / 3	University of Vienna: institution h-index 851 (OpenAlex)
Multicenter collaboration	2 / 3	OpenAlex lists 9 institution(s) in 7 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 29441009)
Free to read	2 / 2	Free to read
Total	50 / 100	—

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

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

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