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40/100

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Inflammation and the immune system

Topic: Amyloid, tau and blood-test diagnosis

One hundred and eighteen years have passed since Alzheimer's disease (AD) was first diagnosed by Alois Alzheimer as a multifactorial and complex neurodegenerative disorder with psychiatric components. It is inaugurated by a cascade of events initiating from amnesic-type memory impairment leading to the gradual loss of cognitive and executive capacities. Pathologically, there is overwhelming evidence that clumps of misfolded amyloid-β (Aβ) and hyperphosphorylated tau protein aggregate in the brain. These pathological processes lead to neuronal loss, brain atrophy, and gliosis culminating in neurodegeneration and fueling AD. Thus, at a basic level, abnormality in the brain's protein function is observed, causing disruption in the brain network and loss of neural connectivity. Nevertheless, AD is an aging disorder caused by a combination of age-related changes and genetic and environmental factors that affect the brain over time. Its mysterious pathology seems not to be limited to senile plaques (Aβ) and neurofibrillary tangles (tau), but to a plethora of substantial and biological processes, which have also emerged in its pathogenesis, such as a breakdown of the blood-brain barrier (BBB), patients carrying the gene variant APOE4, and the immuno-senescence of the immune system. Furthermore, type 2 diabetes (T2DM) and metabolic syndrome (MS) have also been observed to be early markers that may provoke pathogenic pathways that lead to or aggravate AD progression and pathology. There are numerous substantial AD features that require more understanding, such as chronic neuroinflammation, decreased glucose utilization and energy metabolism, as well as brain insulin resistance (IR). Herein, we aim to broaden our understanding and to connect the dots of the multiple comorbidities and their cumulative synergistic effects on BBB dysfunction and AD pathology. We shed light on the path-physiological modifications in the cerebral vasculature that may contribute to AD pathology and cognitive decline prior to clinically detectable changes in amyloid-beta (Aβ) and tau pathology, diagnostic biomarkers of AD, neuroimmune involvement, and the role of APOE4 allele and AD-IR pathogenic link-the shared genetics and metabolomic biomarkers between AD and IR disorders. Investment in future research brings us closer to knowing the pathogenesis of AD and paves the way to building prevention and treatment strategies.

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APA 7th

Bowirrat, A., Pinhasov, A., Bowirrat, A., & Badgaiyan, R. D. (2025). Navigation Between Alzheimer’s Disease (AD) and Its Various Pathophysiological Trajectories: The Pathogenic Link to Neuroimmunology—Genetics and Neuroinflammation. International Journal of Molecular Sciences. https://doi.org/10.3390/ijms26178253

Vancouver

Bowirrat A, Pinhasov A, Bowirrat A, Badgaiyan RD. Navigation Between Alzheimer’s Disease (AD) and Its Various Pathophysiological Trajectories: The Pathogenic Link to Neuroimmunology—Genetics and Neuroinflammation. International Journal of Molecular Sciences. 2025. doi:10.3390/ijms26178253. PMID: 40943177.

BibTeX

@article{bowirrat2025-40943177,
  author  = {Bowirrat, Abdalla and Pinhasov, Albert and Bowirrat, Aia and Badgaiyan, Rajendra Dhar},
  title   = {{Navigation Between Alzheimer’s Disease (AD) and Its Various Pathophysiological Trajectories: The Pathogenic Link to Neuroimmunology—Genetics and Neuroinflammation}},
  journal = {International Journal of Molecular Sciences},
  year    = {2025},
  doi     = {10.3390/ijms26178253},
  pmid    = {40943177},
  url     = {https://doi.org/10.3390/ijms26178253}
}

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Key findings

Furthermore, type 2 diabetes (T2DM) and metabolic syndrome (MS) have also been observed to be early markers that may provoke pathogenic pathways that lead to or aggravate AD progression and pathology.
There are numerous substantial AD features that require more understanding, such as chronic neuroinflammation, decreased glucose utilization and energy metabolism, as well as brain insulin resistance (IR).
Herein, we aim to broaden our understanding and to connect the dots of the multiple comorbidities and their cumulative synergistic effects on BBB dysfunction and AD pathology.
We shed light on the path-physiological modifications in the cerebral vasculature that may contribute to AD pathology and cognitive decline prior to clinically detectable changes in amyloid-beta (Aβ) and tau pathology, diagnostic biomarkers of AD, neuroimmune involvement, and the role of APOE4 allele and AD-IR pathogenic link-the shared genetics and metabolomic biomarkers between AD and IR disorders.
Investment in future research brings us closer to knowing the pathogenesis of AD and paves the way to building prevention and treatment strategies.

Why it matters

This review discusses how neuroinflammation, genetics such as APOE4, blood-brain barrier breakdown, and conditions like type 2 diabetes may contribute to Alzheimer's disease. It is a broad overview, not a new treatment or cure, and it does not report a tested therapy.

Study details

Evidence strengthLow

How this study scored 40/100

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 (International Journal of Molecular Sciences)
Journal's citation record	3 / 4	International Journal of Molecular Sciences: journal h-index 426 (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 5 times (OpenAlex, 2026-10-10)
Citations per year	1 / 5	1.7 citations a year over 3 year(s) since 2025
Impact for its field and year	2 / 6	Cited 2.7× 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 5 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	2 / 4	Last-listed author Rajendra Dhar Badgaiyan: h-index 35 (OpenAlex, whole career)
Institution's track record	1 / 3	Tel Aviv University: institution h-index 1,018 (OpenAlex)
Multi-centre collaboration	2 / 3	OpenAlex lists 5 institution(s) in 2 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 40943177)
Free to read	2 / 2	Free to read
Total	40 / 100	—

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

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