Cerebral "microvascular" disease occurs in lacunar stroke, leukoaraiosis, vascular dementia and Alzheimer's disease. 3 key findings →
Participants: 1,953 Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The 52 baseline participants comprised autosomal dominant Alzheimer's disease mutation carriers (n = 11; 49.6 ± 10.3 years old) and non-carriers (n = 16; 51.1 ± 14.2 years old; 10 male), and patients with sporadic mild cognitive impairment (n = 17; 61.9 ± 6.4 years old; nine male) and sporadic Alzheimer's disease (n = 8; 63.0 ± 6.5 years old; five male); for confidentiality reasons, the gender of mutation carriers is not revealed. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Previous studies of Aβ plasma as a biomarker for Alzheimer's disease (AD) obtained conflicting results. 5 key findings →
Design: longitudinal study Participants: 715 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Glia have been implicated in Alzheimer's disease (AD) pathogenesis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We investigated the effect of crenezumab, a humanized anti-amyloid-beta (Aβ) immunoglobulin (Ig)G4 monoclonal antibody, on biomarkers of amyloid pathology, neurodegeneration, and disease progression in patients with mild-to-moderate Alzheimer's disease (AD). 4 key findings →
Participants: 26 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Central immunity components especially microglia in dementia have been well studied and corresponding immunotherapy gradually caught the attention. 4 key findings →
Design: longitudinal study Participants: 361,653 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Increasing evidence suggests an association between pro-inflammatory diets and cognitive function. 4 key findings →
Design: cohort study Participants: 1,372 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
One hundred eighty-seven participants with brain autopsy (NPDx1: AD n = 85; other n = 102; mean age: 74.3 years, 38.5% female; interval blood collection-death [mean ± SD]: 2.8 ± 1.6 years) and 67 NC without brain autopsy (mean age: 66.5 years, 71.6% female) were included. pTau217, but not GFAP, levels increased stepwise with increasing Thal phases (β = 0.61; 95% CI [0.24-0.97] to β = 0.91 [0.55-1.27]) and Braak stages (β = 0.59; [0.16-1.01] to β = 0.74 [0.33-1.15]). 5 key findings →
Design: cohort study Participants: 85 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A recent randomized trial demonstrated clear cerebrospinal-fluid DHA target engagement without detectable improvement in cognition or brain volume over 24 months. 5 key findings →
Design: randomized controlled trial Evidence: high
Full summary, score breakdown and related studies → Original source
Tau is common in LBD and may reduce clinical diagnostic accuracy in people with DLB. 2 key findings →
Design: meta-analysis Participants: 1,511 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
66/100
Alzheimer's disease (AD) is a debilitating, chronic neurodegenerative disease. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
We found that common variation at the CR1 locus has a broad impact on cognition and that this effect is largely mediated by an individual's amyloid plaque burden. 4 key findings →
Design: cohort study Participants: 1,666 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Recent literature shows that GLP-1 and its agonists, DPP-4 inhibitors and combined GLP-1/GIP molecules are effective in partially or fully reversing the effects of neurotoxic compounds, neurovascular complications of diabetes, neuropathological changes related with Alzheimer's disease, Parkinson's disease or vascular occlusion. 4 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Florbetaben scans were assessed visually and quantitatively, and results were compared with amyloid plaque scores. 3 key findings →
Design: open-label trial Participants: 82 Evidence: low
Full summary, score breakdown and related studies → Original source
NFTs in the substantia nigra are associated with gait impairment in older persons with and without dementia. 4 key findings →
Design: longitudinal study Participants: 86 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Layer II of the entorhinal cortex contains the cells of origin for the perforant path, plays a critical role in memory processing, and consistently degenerates in end-stage Alzheimer's disease. 5 key findings →
Design: longitudinal study Participants: 29 Evidence: moderate
Full summary, score breakdown and related studies → Original source
At baseline, 283 were Plasma-/PET-, 97 Plasma+/PET-, 76 Plasma-/PETLow, and 51 Plasma+/PETLow. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
There is clinical overlap between presentations of dementia due to limbic-predominant age-related TDP-43 encephalopathy (LATE) and Alzheimer's disease. 4 key findings →
Design: longitudinal study Participants: 78 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The mechanisms by which the apolipoprotein E ε4 (APOEε4) allele influences the pathophysiological progression of Alzheimer's disease (AD) are poorly understood. 2 key findings →
Design: longitudinal study Participants: 94 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This trial tested an antibody targeting tau tangles rather than amyloid plaques, in people with mild-to-moderate Alzheimer's. It slowed decline on one cognitive test by 42% compared with placebo, the first time an anti-tau antibody showed any cognitive benefit, but it did not help with daily-function scores, overall dementia staging (CDR-SB), or the MMSE, and it did not reduce tangle buildup seen on tau brain scans. 5 key findings →
Design: phase-2-trial Participants: 272 Evidence: preliminary
Full summary, score breakdown and related studies → Original source
65/100
Alzheimer's disease (AD) therapies utilizing amyloid-β (Aβ) immunization have shown potential in clinical trials. 2 key findings →
Design: case-control Evidence: early
Full summary, score breakdown and related studies → Original source Free full text
65/100
Previous studies have shown that limbic-predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) increases with age, but there have been only a few studies, which have investigated this entity in a population-based setting. 5 key findings →
Design: cohort Participants: 295 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
65/100
This study examined whether levels of blood biomarkers of amyloid (Aβ 42 /Aβ 40 ratio), tau (p-tau 181 ), neurodegeneration (NfL), and glial activation and neuroinflammation (glial fibrillary acidic protein [GFAP], YKL40, soluble triggering receptor expressed on myeloid cells 2 [sTREM2]) collected when participants were cognitively normal are associated with the time to onset of MCI. 5 key findings →
Design: longitudinal study Participants: 271 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Greater neighborhood disadvantage was associated with elevated inflammatory and AD CSF biomarkers cross-sectionally and longitudinal increases in a nonspecific inflammatory blood biomarker. 5 key findings →
Design: longitudinal study Participants: 334 Evidence: moderate
Full summary, score breakdown and related studies → Original source
APOE4 is the strongest genetic risk factor for late-onset Alzheimer disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
From across this tag
10 of the 6,890 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Integrative multi-omic profiling of adult mouse brain endothelial cells and potential implications in Alzheimer's disease
- Mediterranean Diet and Neurodegenerative Diseases: Recent Advances from the Gut–Immune–Brain Axis to Multi-Omics-Guided Precision Nutrition
- Nitric oxide in cell survival: a janus molecule
- Neuroprotective action of resveratrol
- Insulin Resistance is Associated with Higher Cerebrospinal Fluid Tau Levels in Asymptomatic APOEɛ4 Carriers
- Identification of Vulnerable Cell Types in Major Brain Disorders Using Single Cell Transcriptomes and Expression Weighted Cell Type Enrichment
- Chronic neuroinflammation in rats reproduces components of the neurobiology of Alzheimer's disease
- SHP2 in microglia attenuates neuroinflammation and cognitive deficits in vascular dementia by modulating the FAK/Src/PU. 1/IRF8 pathway
- Poly(ADP-Ribose) Prevents Pathological Phase Separation of TDP-43 by Promoting Liquid Demixing and Stress Granule Localization
- Diabetes mellitus and dementia
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 →