Immunity has been suggested to be important in the pathogenesis of dementia. 4 key findings →
Participants: 8,313 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The shared role of amyloid-β (Aβ) deposition in cerebral amyloid angiopathy (CAA) and Alzheimer disease (AD) is arguably the clearest instance of crosstalk between neurodegenerative and cerebrovascular processes. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neuronal and glial cell interaction is essential for synaptic homeostasis and may be affected in Alzheimer's disease (AD). 4 key findings →
Participants: 36 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Prognostic discussions between caregivers of PwD and the PwD's physicians may be occurring more often; however, a high percentage of caregivers report a poor understanding about the terminal nature of dementia and the role of PC. 3 key findings →
Design: cross-sectional Participants: 80 Evidence: moderate
Full summary, score breakdown and related studies → Original source
At baseline, subjects with normal vs. impaired cognition show no notable difference in microbiome diversity but several unique microbial signatures are detected in subjects with mild cognitive impairment. 3 key findings →
Participants: 17 Evidence: high
Full summary, score breakdown and related studies → Original source
55/100
Elevated baseline plasma NfL is a prognostic marker of cognitive decline and neuroimaging measures of neurodegeneration, and has similar effect sizes to baseline CSF NfL. 4 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
The Lumipulse G assays show a very good analytical performance that makes them well-suited for CSF clinical routine measurements. 4 key findings →
Participants: 80 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These findings indicate that plasma NfL is a proxy for neurodegeneration in AD-related regions in Aβ+ subjects. 2 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our findings indicate that AD patients present impairments in some key functional abilities, such as gait, turning and sitting, sit to stand, and reaction time, both in mild and moderate AD. 4 key findings →
Design: cross-sectional Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source
Studies of rodent models of Alzheimer's disease (AD) and of human tissues suggest that the retinal changes that occur in AD, including the accumulation of amyloid beta (Aβ), may serve as surrogate markers of brain Aβ levels. 3 key findings →
Participants: 15 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Research into the role of the gut microbiome in modulating brain function has rapidly increased over the past 10 years, albeit chiefly in animal models. 5 key findings →
Design: cross-sectional Evidence: high
Full summary, score breakdown and related studies → Original source
Previous studies demonstrated that plasma neurofilament light chain (NFL) played important predictive roles in disease progression and neurodegeneration in the preclinical phase of familial Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) tau and phosphorylated tau (ptau) are definite biomarkers of Alzheimer's disease (AD). 1 key finding →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
APOE-ε4 carrier status appears to modify the cross-sectional association between cardiac output and neuropsychological performance such that lower cardiac output relates to poorer performances among carriers of the ε4 allele. 3 key findings →
Design: cross-sectional Participants: 306 Evidence: low
Full summary, score breakdown and related studies → Original source
Hippocampal atrophy rate has been correlated with cognitive decline and its genetic modifiers are still unclear. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Two novel SNPs (rs465401 and rs460420), both near the ADAMTS1 gene on chromosome 21, showed genome-wide significant associations with CSF NFL. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
55/100
Mild-cognitive impairment (MCI) occurs in up to one-fifth of individuals over the age of 65, with approximately a third of MCI individuals converting to dementia in later life. 2 key findings →
Participants: 122 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We examined the relationships between amyloid-β PET and concurrent and longitudinal cognitive performance in 107 cognitively normal individuals with subjective cognitive decline (age: 64 ± 8 years, 44% female, Mini-Mental State Examination score 29 ± 1). 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The combined model (Harrell's C = 0.82 [0.78-0.86]) was significantly superior to demographics (β = 0.100, P < .001), magnetic resonance imaging (β = 0.037, P = .011), and PET only models (β = 0.053, P = .003).The models can be used to calculate individualized risk, for example, a female MCI patient (age = 60, APOE ε4 positive, Mini-Mental State Examination = 25, hippocampal volume = 5.8 cm3, amyloid PET positive) has 35% (19-57) risk in one year and 85% (64-97) risk in three years. 3 key findings →
Participants: 411 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Aging is associated with decline in white matter (WM) microstructure, decreased cognitive functioning, and increased risk of Alzheimer's disease and related dementias. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
55/100
Totally 30,332 patients (5.6%) were diagnosed with dementia during the follow-up, with 14,097 men (4.9%) and 16,235 women (6.5%). 5 key findings →
Participants: 537,513 Evidence: low
Full summary, score breakdown and related studies → Original source
55/100
Atrial fibrillation (AF) is one of the cardiovascular risk factors for dementia. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
RECENT FINDINGS: Evidence to date supports the notion that higher levels of CR, as measured by proxy variables reflective of lifetime experiences, are associated with better cognitive performance, and with a reduced risk of incident mild cognitive impairment/dementia. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The concept of cognitive reserve (CR) was proposed to account for the discrepancy between levels of brain pathologic process or damage and clinical and cognitive function. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Educational attainment is widely accepted as a cognitive reserve variable. 2 key findings →
Design: longitudinal study 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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →