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

Find studies

Showing 15,751–15,775 of 27,146 studies marked Peer-reviewed (page 631 of 1086) · 28,180 in the whole library · How the 0–100 score works

Download bibliography of the first 500 of these 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.

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.

Cells expressing leucocyte common antigen (LCA) as well as T-cytotoxic-suppressor (T8) and T-helper-inducer (T4) antigens were detected in significant numbers in the hippocampus and temporal cortex of Alzheimer but not normal brain tissue. 4 key findings →

Evidence: low

Neuroinflammation has an established link with AIDS-related dementia but has not been investigated in the post-highly active anti-retroviral therapy (HAART) era. 4 key findings →

Evidence: low

MHC class II-positive microglia in human brain: association with Alzheimer lesions

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Journal of neuroscience research 1992-12-01

Cells of the mononuclear phagocytic system (MPS) present foreign antigen on their cell surfaces bound to major histocompatibility complex (MHC) class II molecules. 4 key findings →

Evidence: low

Human TBK1: A Gatekeeper of Neuroinflammation

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Trends in molecular medicine 2016-06-01

The importance of TANK binding kinase-1 (TBK1), a multimeric kinase that modulates inflammation and autophagy, in human health has been highlighted for the first time by the recent discoveries of mutations in TBK1 that underlie amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), normal tension glaucoma (NTG) or childhood herpes simplex encephalitis (HSE). 3 key findings →

Evidence: low

Reactive microgliosis, hallmark of neuroinflammation, may contribute to neuronal degeneration, as shown in several neurodegenerative diseases. 4 key findings →

Evidence: low

Alzheimer's disease as an inflammatory disease

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Biomolecular concepts 2017-03-01

Alzheimer's disease (AD) is a neurodegenerative condition characterized by the formation of amyloid-β plaques, aggregated and hyperphosphorylated tau protein, activated microglia and neuronal cell death, ultimately leading to progressive dementia. 2 key findings →

Evidence: low

Vascular dementia (VD) is defined as a progressive neurodegenerative disease of cognitive decline, attributable to cerebrovascular factors. 4 key findings →

Evidence: low

Peripheral benzodiazepine receptor (PBR) in the brain of Alzheimer's disease (AD) patients has been discussed in relation to the role of gliosis in AD. 4 key findings →

Evidence: low

Cerebral vascular amyloid beta-protein (Abeta) deposition, also known as cerebral amyloid angiopathy, is a common pathological feature of Alzheimer's disease. 4 key findings →

Evidence: low

Women living in areas with higher walkability showed slower rates of decline in immediate (estimate=0.019, SE=0.009) and delayed recall (estimate=0.018, SE=0.008) (Figure 1). 5 key findings →

Design: longitudinal study Evidence: moderate

Five overarching themes derived from the interviews were as follows: (a) My life still has value and meaning, (b) I am my own unique individual, (c) I place my trust in other people, (d) The future worries me, and (e) I accept and embrace what life brings. 5 key findings →

Evidence: low

Per-dyad mean cost savings at 12 months were $2 354 for those who received COPE with a mean difference-in-difference of -$6 667 versus HCBS alone (95% CI: -$15 473, $2 734; not statistically significant). 4 key findings →

Evidence: low

Using the time-dependent Cox model, the adjusted dementia rate ratios (95% confidence-interval) among current and former users were 0.90(0.70-1.16) and 0.89 (0.71-1.10), respectively. 3 key findings →

Design: longitudinal study Evidence: moderate

The agreement between the two measures of dementia differed by age: in 2017, 79.2% of hospital claims for patients aged 66–74 had a diagnosis of dementia compared to older age categories that had dementia noted in over 85% of records. 5 key findings →

Participants: 1,273,348 Evidence: low

Role of PCPs in diagnosing dementia in traditional Medicare and Medicare Advantage

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Alzheimer s & Dementia 2025-10-01

Among a matched sample of 15,410,030 beneficiaries, accounting for both provider and patient characteristics, the incident dementia diagnosis rate was 0.11 percentage points lower for MA beneficiaries compared to TM beneficiaries attributed to the same PCP. 5 key findings →

Evidence: moderate

This study examines the difference in functional outcomes among Traditional Medicare (TM) and Medicare Advantage (MA) beneficiaries with Alzheimer’s disease and related dementias (ADRD) during a home health admission, which is unknown. 5 key findings →

Design: cohort study Participants: 81,735 Evidence: moderate

Among 421,131 MA beneficiaries, telehealth use increased sharply in Q2 2020 for both ADRD and non-ADRD groups, peaking at 33.9 and 30.6% respectively. 5 key findings →

Design: cohort study Evidence: moderate

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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. Show only studies that are free to read

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
  • Randomised / 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
  • Multi-centre 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.

1,034 records (3.7% of the library) are not peer-reviewed — 962 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