Full summary, score breakdown and related studies → Original source Free full text
Research
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Neurotoxic amyloid beta peptide (Abeta) accumulates in the brains of individuals with Alzheimer disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The findings suggest that GPS driving may serve as an effective and accurate digital biomarker for identifying preclinical AD among older adults. 2 key findings →
Participants: 64 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Emerging evidence supports a role for innate immunity and microglia in Alzheimer's disease (AD) pathophysiology. 4 key findings →
Participants: 218 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is characterized by plaques containing amyloid-β (Aβ) and neurofibrillary tangles composed of aggregated, hyperphosphorylated tau. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In Alzheimer's disease (AD) models, AD risk variants in the microglial-expressed TREM2 gene decrease Aβ plaque-associated microgliosis and increase neuritic dystrophy as well as plaque-associated seeding and spreading of tau aggregates. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
White matter alterations are present in the majority of patients with Alzheimer's disease type dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Variants in the triggering receptor expressed on myeloid cells 2 (TREM2) gene are associated with increased risk for late-onset AD. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
CSF SDC4 levels were elevated in AD, including the earliest preclinical stages, compared to controls and were closely associated with CSF and imaging biomarkers of amyloid and tau, and CSF biomarkers of neuronal and synaptic injury, astrocytic reactivity and microglial dysregulation. 1 key finding →
Design: cross-sectional Participants: 1,041 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the leading cause of dementia and is characterized by progressive amyloid accumulation followed by tau-mediated neurodegeneration. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease is more than a pure proteopathy. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Soluble triggering receptor expressed on myeloid cells 2 (sTREM2) in cerebrospinal fluid (CSF) has been associated with Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The apolipoprotein E4 (APOE4) allele is associated with an increased risk of Alzheimer disease and a decreased risk of glaucoma, but the underlying mechanisms remain poorly understood. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dietary habits and vascular risk factors promote both Alzheimer's disease and cognitive impairment caused by vascular factors 1-3 . 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Moreover, the presence of Aβ+ was associated with an elevated [18F]-AV-1451 SUVR in AD cortical signature regions (Aβ+ participants: mean [SD], 1.3 [0.3]; Aβ- participants: 1.1 [0.1]; F = 4.3, P = .04) but not in the hippocampus. 3 key findings →
Participants: 59 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The defining feature of Parkinson disease (PD) and Lewy body dementia (LBD) is the accumulation of alpha-synuclein (Asyn) fibrils in Lewy bodies and Lewy neurites. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neuropsychiatric symptoms (NPSs) are hallmarks of Alzheimer's disease (AD), causing substantial distress for both people with dementia and their caregivers, and contributing to early institutionalization. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the leading cause of dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the sixth leading cause of death in the United States and the most common cause of dementia in the elderly. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Many genetic studies for Alzheimer's disease (AD) have been focused on the identification of common genetic variants associated with AD risk and not on other aspects of the disease, such as age at onset or rate of dementia progression. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Tauopathies are a broad set of neurodegenerative dementias characterized by aggregation of the tau protein into filamentous inclusions that can be found in neurons and glial cells. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Full summary, score breakdown and related studies → Original source Free full text
Apolipoprotein E (ApoE) is of great interest due to its role as a cholesterol/lipid transporter in the central nervous system (CNS) and as the most influential genetic risk factor for Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our findings highlight the value of transethnic studies for identifying novel AD susceptibility loci. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The apolipoprotein E E4 allele of the APOE gene is the strongest genetic factor for late-onset Alzheimer disease (LOAD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →