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39/100

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Inflammation and the immune system

Topic: Amyloid, tau and blood-test diagnosis

Plain-language summary

The brain contains approximately 100 billion neurons and over 200 billion glial cells, which are integral to the neuronal networks that support normal brain function in the central nervous system. The complexity of the brain makes the diagnosis and treatment of neurodegenerative disease particularly challenging. Neuroinflammation and neuronal cell death contribute to the development of neurodegenerative diseases such as dementia. Dementia refers to a decline in memory and thinking ability, affecting approximately 55 million people worldwide. Owing to the association of multiple factors, including amyloid- β plaque, tau-fibrillary tangles, neuroinflammation, nutritional defects, and genetic mutations, the exact cause of the most common type of dementia, Alzheimer’s disease, remains elusive. These multiple factors may cause damage to neurons and glial cells, leading to neurodegeneration. Very few therapeutics are available for neurodegenerative diseases due to the limited understanding of their pathogenesis, resulting in the lack of biomarkers and drug targets. Recent attention has shifted toward addressing modifiable risk factors such as unhealthy diets and lifestyles to delay the onset of Alzheimer’s disease. Unhealthy diets that consist of saturated fatty acids and refined sugars, with other multiple risk factors, increase neuroinflammation and oxidative stress, furthering cognitive decline and progression of neurodegeneration. Mitigating these risk factors with antioxidants, anti-inflammatory-based nutrition, and multidomain lifestyle intervention, which may include physical exercise, cognitive stimulation, and social engagement, may delay the development of neurodegenerative diseases and cognitive decline. In this review, we focus on the role of neuroinflammation in contributing to neurodegeneration and dietary influence in Alzheimer’s disease.

What this study adds

Evidence grade: Low

This review discusses how unhealthy diets high in saturated fats and refined sugars increase neuroinflammation and oxidative stress and notes that attention has shifted to modifiable risk factors to delay Alzheimer's onset. It does not show that any dietary change prevents or treats the disease.

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

Park, H., Ni, M., & Le, Y. (2025). Neuroinflammation and nutrition in Alzheimer’s disease. Frontiers in Neurology. https://doi.org/10.3389/fneur.2025.1622571

Vancouver

Park H, Ni M, Le Y. Neuroinflammation and nutrition in Alzheimer’s disease. Frontiers in Neurology. 2025. doi:10.3389/fneur.2025.1622571. PMID: 40771977.

BibTeX

@article{park2025-40771977,
  author  = {Park, Hyoungshin and Ni, Manting and Le, Yvonne},
  title   = {{Neuroinflammation and nutrition in Alzheimer’s disease}},
  journal = {Frontiers in Neurology},
  year    = {2025},
  doi     = {10.3389/fneur.2025.1622571},
  pmid    = {40771977},
  url     = {https://doi.org/10.3389/fneur.2025.1622571}
}

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.

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.

New to reading papers? Six questions to ask of any Alzheimer’s study · how we score.

Key findings

Very few therapeutics are available for neurodegenerative diseases due to the limited understanding of their pathogenesis, resulting in the lack of biomarkers and drug targets.
Recent attention has shifted toward addressing modifiable risk factors such as unhealthy diets and lifestyles to delay the onset of Alzheimer’s disease.
Unhealthy diets that consist of saturated fatty acids and refined sugars, with other multiple risk factors, increase neuroinflammation and oxidative stress, furthering cognitive decline and progression of neurodegeneration.
Mitigating these risk factors with antioxidants, anti-inflammatory-based nutrition, and multidomain lifestyle intervention, which may include physical exercise, cognitive stimulation, and social engagement, may delay the development of neurodegenerative diseases and cognitive decline.
In this review, we focus on the role of neuroinflammation in contributing to neurodegeneration and dietary influence in Alzheimer’s disease.

Why it matters

Study details

Evidence strengthLow

How this study scored 39/100

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. We have no data on senior author's track record, so that was left out: it earned 37 of the 96 points we could judge it on, which is 39 out of 100.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Frontiers in Neurology)
Journal's citation record	2 / 4	Frontiers in Neurology: journal h-index 162 (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)
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	2 / 7	Cited 12 times (OpenAlex, 2026-10-10)
Citations per year	2 / 5	4.0 citations a year over 3 year(s) since 2025
Impact for its field and year	3 / 6	Cited 6.6× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	1 / 6	Cited by 2 other studies in this library
Still being cited	1 / 4	Cited 12 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	— / 4	Senior author's record not available — left out of this score
Institution's track record	0 / 3	Massachusetts College of Pharmacy and Health Sciences: institution h-index 157 (OpenAlex)
Multicenter 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 40771977)
Free to read	2 / 2	Free to read
Points	37 / 96	Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 37 of the 96 points we could judge it on is 39 out of 100.
Total	39 / 100	—

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

Read the original

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