alzhub.org
Get help now — free helplines

You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

In a medical emergency, call 911. More numbers, and what each line does, on the help page.

Research

31,780 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1–25 of 40 studies in Inflammation and the immune system · free to read · tagged Treatments (page 1 of 2) · 31,780 in the whole library · How the 0–100 score works

Download bibliography of these 40 studies, in this order: BibTeX (.bib) · RIS (.ris)

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

Other subjects

Authors

Names as each record prints them; the same person can appear under two spellings.

Institutions

From OpenAlex; 17,251 studies have no institution on record and are not counted here.

What “Inflammation and the immune system” covers

Inflammation and the immune system — The brain's immune cells and inflammatory signals, and their role in how Alzheimer's starts and progresses.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

evoke and evoke+: design of two large-scale, double-blind, placebo-controlled, phase 3 studies evaluating efficacy, safety, and tolerability of semaglutide in early-stage symptomatic Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 81 out of 100. Alzheimer's research & therapy 2025-01-08

Enrollment was undertaken between May 18, 2021, and September 8, 2023. 2 key findings →

Design: clinical trial Participants: 210 Evidence: high

Full summary, score breakdown and related studies → Original source Free full text

Natural compounds as multitarget agents in Alzheimer's diseases: evidence from in vivo and in vitro models

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Frontiers in pharmacology 2026-02-23

Overall, the available evidence suggests that natural compounds confer multitarget neuroprotective effects that directly engage with key pathological mechanisms underlying AD. 4 key findings →

Design: systematic review Participants: 41 Evidence: high

Full summary, score breakdown and related studies → Original source Free full text

Effect of antidiabetic drugs in Alzheimer´s disease: a systematic review of preclinical and clinical studies

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Molecular neurodegeneration 2025-10-27

The potential neuroprotective effects of antidiabetic treatments have been largely assessed in Alzheimer's disease (AD) and AD-like dementia models, with or without metabolic disorders. 1 key finding →

Design: systematic review Participants: 405 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

[The role of antidiabetic drugs in the treatment of Alzheimer's disease: systematic review]

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Problemy endokrinologii 2023-11-11

Recent studies show that Alzheimer's disease (AD) has many common links with conditions associated with insulin resistance, including neuroinflammation, impaired insulin signaling, oxidative stress, mitochondrial dysfunction and metabolic syndrome. 5 key findings →

Design: meta-analysis Evidence: high

Full summary, score breakdown and related studies → Original source Free full text

Biomarkers and therapeutic strategies targeting microglia in neurodegenerative diseases: current status and future directions

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Molecular Neurodegeneration 2025-07-10

Recent advances in our understanding of non-cell-autonomous mechanisms in neurodegenerative diseases (NDDs) have highlighted microglial dysfunction as a core driver of disease progression. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Microglial activation and beta -amyloid deposit reduction caused by a nitric oxide-releasing nonsteroidal anti-inflammatory drug in amyloid precursor protein plus presenilin-1 transgenic mice

✓ Peer-reviewed alzhub usefulness score 48 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2002-03-01

3-4-(2-Fluoro-alpha-methyl-[1,1'-biphenyl]-4-acetyloxy)-3-methoxyphenyl]-2-propenoic acid 4-nitrooxy butyl ester (NCX-2216), a nitric oxide (NO)-releasing derivative of the cyclooxygenase-1-preferring nonsteroidal anti-inflammatory drug (NSAID) flurbiprofen, dramatically reduced both beta-amyloid (Abeta) loads and Congo red staining in doubly transgenic (Tg) amyloid precursor protein plus presenilin-1 mice when administered at 375 ppm in diet between 7 and 12 months of age. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Next-generation active immunization approach for synucleinopathies: implications for Parkinson's disease clinical trials

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Acta neuropathologica 2014-02-14

Immunotherapeutic approaches are currently in the spotlight for their potential as disease-modifying treatments for neurodegenerative disorders. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Drug repositioning and repurposing for Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Nature reviews. Neurology 2020-09-16

Drug repositioning and repurposing can enhance traditional drug development efforts and could accelerate the identification of new treatments for individuals with Alzheimer disease (AD) dementia and mild cognitive impairment. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Cannabinoids for treatment of Alzheimer's disease: moving toward the clinic

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Frontiers in pharmacology 2014-03-05

The limited effectiveness of current therapies against Alzheimer's disease (AD) highlights the need for intensifying research efforts devoted to developing new agents for preventing or retarding the disease process. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Chitinase-3-like-1: a multifaceted player in neuroinflammation and degenerative pathologies with therapeutic implications

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Molecular Neurodegeneration 2025-01-18

Chitinase-3-like-1 (CHI3L1) is an evolutionarily conserved protein involved in key biological processes, including tissue remodeling, angiogenesis, and neuroinflammation. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Neurofilament Biomarkers in Neurology: From Neuroinflammation to Neurodegeneration, Bridging Established and Novel Analytical Advances with Clinical Practice

✓ Peer-reviewed alzhub usefulness score 45 out of 100. International Journal of Molecular Sciences 2025-10-07

Neuroaxonal damage underlies permanent disability in various neurological conditions, both neuroautoimmune and neurodegenerative. 5 key findings →

Design: narrative review Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Neuroinflammation and blood–brain barrier dysfunction in cerebral small vessel disease: mechanisms, biomarkers, and therapeutic implications

✓ Peer-reviewed alzhub usefulness score 45 out of 100. European journal of medical research 2026-01-23

Cerebral small vessel disease (CSVD) is a chronic, progressive cerebrovascular disorder affecting small arteries, arterioles, venules, and capillaries, and is a leading contributor to stroke, vascular dementia, and cognitive impairment. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Dynamic changes in pro- and anti-inflammatory cytokines in microglia after PPAR-γ agonist neuroprotective treatment in the MPTPp mouse model of progressive Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Neurobiology of disease 2014-08-15

Neuroinflammatory changes play a pivotal role in the progression of Parkinson's disease (PD) pathogenesis. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

A Systematic Review to Evaluate the Effect of Neflamapimod on Cognitive Function and Progression of Dementia

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Neurology India 2026-01-09

Treatment options for dementia mainly comprise of symptomatic treatment, as no disease-modifying therapy currently exists that directly reduces the pathology. 3 key findings →

Design: systematic review Evidence: high

Full summary, score breakdown and related studies → Original source Free full text

↑ Change the filters

Where “Free full text” comes from

Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled.

How the 0–100 score works — and why some entries are capped

This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.

  • Journal tier up to 10 pts
  • Journal's citation record up to 4 pts
  • Study design up to 12 pts
  • Strength of evidence up to 5 pts
  • Peer-review validation up to 10 pts
  • How recent up to 5 pts
  • Sample size up to 4 pts
  • Effect reported up to 3 pts
  • Studied in people up to 3 pts
  • Randomized / blinded up to 2 pts
  • Times cited up to 7 pts
  • Citations per year up to 5 pts
  • Impact for its field and year up to 6 pts
  • Cited by studies here up to 6 pts
  • Still being cited up to 4 pts
  • Senior author's track record up to 4 pts
  • Institution's track record up to 3 pts
  • Multicenter collaboration up to 3 pts
  • Indexed in PubMed up to 2 pts
  • Free to read up to 2 pts

Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.

Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.

We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.

The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.

See the whole rubric drawn out → — four charts covering all 31,780 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.

What this library is — and isn't

This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 31,780 records, built mostly from automated pulls of Europe PMC (66% of the library) and OpenAlex (16%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.

1,052 records (3.3% of the library) are not peer-reviewed — 973 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.

See the full, machine-readable breakdown of this library's coverage →

Newest studies, as a dated timeline →    Atom feed    Where this research is being discussed: events