The pattern of deficits across tasks was qualitatively compared with normal age-related decline, and early-stage dementia. 3 key findings →
Participants: 460 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.
Repetitive head trauma is a risk factor for Alzheimer's disease and is the primary cause of chronic traumatic encephalopathy. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our study is well placed to evaluate the clinical utility of RMT assessments. 3 key findings →
Participants: 220 Evidence: low
Full summary, score breakdown and related studies → Original source
The ICA demonstrated convergent validity with MoCA (Pearson r=0.58, p<0.0001) and ACE (r=0.62, p<0.0001). 5 key findings →
Participants: 230 Evidence: low
Full summary, score breakdown and related studies → Original source
Differences in expressing facial emotions are broadly observed in people with cognitive impairment. 3 key findings →
Participants: 493 Evidence: low
Full summary, score breakdown and related studies → Original source
Previous studies have shown that the diagnostic performance of digital cognitive tests is comparable with that of conventional paper-and-pencil tests. 3 key findings →
Participants: 54 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The major known genetic risk for Alzheimer's disease (AD), apolipoprotein E-4 (APOE-4), is associated with lowered parietal, temporal, and posterior cingulate cerebral glucose metabolism in patients with a clinical diagnosis of AD. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
We identified a PSEN1 (presenilin 1) mutation carrier from the world's largest autosomal dominant Alzheimer's disease kindred, who did not develop mild cognitive impairment until her seventies, three decades after the expected age of clinical onset. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
By multiple logistic regression, the APOE-epsilon 4 allele frequency was significantly higher in the patients positive for HSV1 in brain than in the HSV1-negative AD group, the HSV1-positive non-AD group, or the HSV1-negative non-AD group (52.8% vs 10.0%, 3.6%, and 6.3%, respectively). 3 key findings →
Participants: 40 Evidence: low
Full summary, score breakdown and related studies → Original source
Corticobasal degeneration (CBD) is a neurodegenerative tauopathy-a class of disorders in which the tau protein forms insoluble inclusions in the brain-that is characterized by motor and cognitive disturbances 1-3 . 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Causes of the well-documented association between low levels of cognitive functioning and many adverse neuropsychiatric outcomes, poorer physical health and earlier death remain unknown. 4 key findings →
Participants: 112 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a complex disorder influenced by environmental and genetic factors. 1 key finding →
Participants: 10,922 Evidence: low
Full summary, score breakdown and related studies → Original source
52/100
We used a collection of 708 prospectively collected autopsied brains to assess the methylation state of the brain's DNA in relation to Alzheimer's disease (AD). 2 key findings →
Participants: 117 Evidence: low
Full summary, score breakdown and related studies → Original source
The role of DNA cytosine methylation, an epigenetic regulator of chromatin structure and function, during normal and pathological brain development and aging remains unclear. 1 key finding →
Participants: 125 Evidence: moderate
Full summary, score breakdown and related studies → Original source
An 8-plex version of an isobaric reagent for the quantitation of proteins using shotgun methods is presented. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
52/100
More specifically, 18F-AV-1451 binding was significantly increased in patients with Alzheimer's disease, relative to patients with progressive supranuclear palsy and with control subjects, in the hippocampus and in occipital, parietal, temporal, and frontal cortices (t's > 2.2, P's < 0.04). 4 key findings →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source
Tau vulnerability in women is not just limited to the medial temporal lobe and significantly contributed to greater risk of faster cognitive decline. 2 key findings →
Participants: 55 Evidence: moderate
Full summary, score breakdown and related studies → Original source
52/100
Cognitive resilience is an important modulating factor of cognitive decline in Alzheimer's disease, but the functional brain mechanisms that support cognitive resilience remain elusive. 4 key findings →
Participants: 108 Evidence: low
Full summary, score breakdown and related studies → Original source
In several neurodegenerative diseases that are collectively called tauopathies, progressive accumulation of tau in the brain is closely associated with neurodegeneration and cognitive impairment. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
52/100
Age-related hippocampal sclerosis may account for a significant proportion of elderly participants with amnestic dementia. 4 key findings →
Participants: 15 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Altered iron metabolism has been hypothesized to be associated with Alzheimer's disease pathology, and prior work has shown associations between iron load and beta amyloid plaques. 5 key findings →
Participants: 421 Evidence: low
Full summary, score breakdown and related studies → Original source
52/100
We found significant group-wise differences in 11C-PK-11195 binding between each patient group and controls in frontotemporal regions, in both a regions-of-interest analysis and in the comparison of principal spatial components of binding. 18F-AV-1451 binding was increased in semantic variant primary progressive aphasia compared to controls in the temporal regions, and both semantic variant primary progressive aphasia and behavioural variant frontotemporal dementia differed from controls in the expression of principal spatial components of binding, across temporal and frontotemporal cortex, respectively. 2 key findings →
Participants: 31 Evidence: low
Full summary, score breakdown and related studies → Original source
Major imaging biomarkers of Alzheimer's disease include amyloid deposition [imaged with [(11)C]Pittsburgh compound B (PiB) PET], altered glucose metabolism (imaged with [(18)F]fluro-deoxyglucose PET), and structural atrophy (imaged by MRI). 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
A decrease of self-confidence about memory abilities in cognitively normal elderly subjects may be related to the neuropathological hallmark of AD measured with PiB-positron emission tomography. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
PiB and FDG showed similar accuracy in discriminating AD and FTLD. 2 key findings →
Participants: 62 Evidence: low
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 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 →