Neuroinflammation is believed to be a key process in Alzheimer's disease (AD) pathogenesis. 5 key findings →
Design: longitudinal study Participants: 1,544 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Research
30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Generalised linear regressions showed significant quadratic associations between amyloid age and cognitive performance and cubic associations between amyloid age and tau, both at baseline and at the 32-month follow-up. 1 key finding →
Design: cohort study Participants: 167 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The limited number of independent cohorts, lack of longitudinal data, and exclusion of individuals with mixed dementia limit the generalizability of these findings. 4 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
In this study, cortical amyloid moderated the association between worsening depressive symptoms and declining cognition in older adults. 4 key findings →
Design: cohort study Participants: 276 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In patients, smaller volumes in a region corresponding to the nucleus basalis of Meynert were associated with greater change in global cognitive, but not motor scores after 2 years. 2 key findings →
Design: longitudinal study Participants: 168 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Over the past two decades, resting-state functional connectivity (RSFC) methods have provided new insights into the network organization of the human brain. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease (AD), amyloid-β (Aβ) triggers the aggregation and spreading of tau pathology, which drives neurodegeneration and cognitive decline. 3 key findings →
Design: cohort Participants: 609 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These results suggest that increasing levels of tau most consistently relate to declines in cognition preceding biomarker collection. 4 key findings →
Design: longitudinal study Participants: 152 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
SUVr abnormality was most frequently observed in cingulate, followed by orbitofrontal, precuneal, and insular cortices and then the associative, temporal, and occipital regions. 1 key finding →
Design: longitudinal study Participants: 867 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In a community-based cohort of 70-year olds, P-NfL was associated with both prevalent and incident CKD, while CSF and/or imaging measures did not differ by CKD status. 3 key findings →
Design: cohort study Participants: 744 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This study shows that PUTG component scores were significantly associated with diagnostic group and AD biomarkers, a finding that was more pronounced in APOE ε4 carriers. 5 key findings →
Design: longitudinal study Participants: 689 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In 135 older adults (mean age = 69.3 years; women = 61.5%), no associations were found within AD-signature regions (all p > 0.25). 3 key findings →
Design: randomized controlled trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
For cognitively unimpaired individuals, living in the most disadvantaged neighborhoods was associated with significantly lower cerebral volumes, after controlling for maximal premorbid (total intracranial) volume. 4 key findings →
Design: cohort study Participants: 951 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Twelve articles-published between the 2007 and 2017-have been included in this systematic review after a quantitative and qualitative selection. 4 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
In this study, elevated [18F]RO948 SUVRs were most often seen among Aβ-positive cases, which suggests that [18F]RO948 has high specificity for AD-type tau and highlights its potential as a diagnostic marker in the differential diagnosis of AD. 4 key findings →
Design: cross-sectional Participants: 257 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
68/100
Our prospective findings provide evidence for what may be an early contributory role of systemic inflammation in neurodegeneration and cognitive aging. 3 key findings →
Design: cohort study Participants: 1,633 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In this study, lower AD signature region volumes, brain microhemorrhages, higher WMH volumes, and infarcts were risk factors associated with dementia in older community-based residents. 4 key findings →
Design: cohort study Participants: 1,553 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
68/100
Arterial stiffness was associated with Aβ plaque deposition in the brain, independent of BP and APOE ε4 allele. 5 key findings →
Participants: 91 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Elecsys CSF biomarker assays may provide reliable alternatives to PET in Alzheimer's disease diagnosis. 3 key findings →
Participants: 277 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Analysis was performed on 115 participants as the full analysis set (probiotic 55, placebo 60). 4 key findings →
Participants: 130 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Although brain neuroinflammation may play an instrumental role in the pathophysiology of Alzheimer's disease, its actual impact on disease progression remains controversial, being reported as either detrimental or protective. 4 key findings →
Design: longitudinal study Participants: 33 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The efficacy, safety and disease-modification of tramiprosate (homotaurine)were investigated in a recently completed large-scale Phase III clinical study in patients with mild to moderate Alzheimer's disease (AD), the Alphase study. 4 key findings →
Design: longitudinal study Participants: 109 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Voxel-wise contrasts against controls (at P < 0.05 family-wise error corrected) showed that (18)F-AV1451 and (18)F-FDG patterns in patients with posterior cortical atrophy ('visual variant of Alzheimer's disease', n = 7) specifically targeted the clinically affected posterior brain regions, while (11)C-PiB bound diffusely throughout the neocortex. 5 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Presence on T2-weighted images of white matter hyperintensities (WMH) has been previously shown to be more commonly associated with GRN mutations rather than other forms of FTD. 5 key findings →
Design: longitudinal study Participants: 336 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Brain volume analyses included 622 participants (mean age ± SD: 70.9 ± 10.2) with an average of 3.3 MRI scans over 4.7 years. 5 key findings →
Design: longitudinal study Participants: 622 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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