31,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Syn positivity (synSAA+) co-occurred with T (in synSAA+ vs. synSAA-, 36% vs. 20% T+; Pp = 0.011) and with cognitive impairment (10% vs. 7% mild cognitive impairment; 10% vs. 0% dementia; p = 0.00050). synSAA+ participants' cognitive performance declined ≈ 40% faster than synSAA- for Digit Symbol Substitution, but not other tests. 4 key findings →
Design: longitudinal study Participants: 420 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Modulating deposition of Aβ-containing plaques in the brain may be beneficial in treating Alzheimer's disease. β-site amyloid precursor protein cleaving enzyme 1 (BACE1) inhibitors have been shown to reduce Aβ in plasma and CSF in healthy volunteers. 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source
Previous post-mortem assessments of TREM2 expression and its association with brain pathologies have been limited by sample size. 3 key findings →
Design: longitudinal study Participants: 945 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease (AD), younger symptom onset is associated with accelerated disease progression and tau spreading, yet the mechanisms underlying faster disease manifestation are unknown. 4 key findings →
Design: longitudinal study Participants: 240 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease, amyloid-beta (Aβ) triggers the trans-synaptic spread of tau pathology, and aberrant synaptic activity has been shown to promote tau spreading. 2 key findings →
Design: longitudinal study Participants: 93 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Neuropathology and neuroimaging studies have identified several subtypes of Alzheimer's disease (AD): hippocampal sparing AD, typical AD, and limbic predominant AD. 2 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Passive immunotherapy in AD is largely dominated by anti-amyloid antibodies, which are more numerous and more advanced in the pipeline. 3 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
GLP-1 RAs positively affect cognitive function in AD patients with T2DM. 4 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Increased levels of triglycerides at midlife predict brain Aβ and tau pathology 20 years later in cognitively healthy individuals. 5 key findings →
Design: cohort study Participants: 134 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Abnormal aggregates of the synaptic protein, α-synuclein, are the dominant pathology in syndromes known as the synucleinopathies. 1 key finding →
Design: meta-analysis Evidence: high
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Parietal cortex RNA-sequencing (RNA-seq) data were generated from individuals with and without Alzheimer disease (AD; n control = 13; n AD = 83) from the Knight Alzheimer Disease Research Center (Knight ADRC). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In older cognitively unimpaired individuals (≥50 years), widespread, age-related elevated tau signal was seen among those with normal or abnormal amyloid status as compared to younger cognitively unimpaired individuals (30-49 years). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There were 987 participants (290 from Vantaa 85+, 241 from the Cambridge City Over-75s Cohort, and 456 from the Cognitive Function and Ageing Study) with neuropathologic data; mean (SD) age at death was 90 (6.4) years, including 682 women (69%). 5 key findings →
Design: cohort study Participants: 987 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Neuropathology was ubiquitous, with 94% of participants having 1+, 78% having 2+, 58% having 3+, and 35% having 4+. 1 key finding →
Design: longitudinal study Participants: 1,079 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Dementia is a severe neurodegenerative disorder and it can be categorized into several subtypes by different pathogenic causes. 3 key findings →
Participants: 10,000 Evidence: low
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Pooled clinical and neuropathologic data from 3 prospective cohort studies indicate that TBI with LOC is associated with risk for Lewy body accumulation, progression of parkinsonism, and PD, but not dementia, AD, neuritic plaques, or neurofibrillary tangles. 5 key findings →
Design: cohort study Participants: 7,130 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The diverse leukocyte infiltrate in atherosclerotic mouse aortas was recently analyzed in 9 single-cell RNA sequencing and 2 mass cytometry studies. 4 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
We tested the hypothesis that cerebral amyloid angiopathy (CAA) is related to Alzheimer disease (AD) dementia and decline in multiple cognitive systems in old age, independent of AD plaque and tangle pathology and other common age-related neuropathologies. 4 key findings →
Design: longitudinal study Participants: 1,113 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's dementia is significantly more common in women than in men. 4 key findings →
Design: longitudinal study Participants: 971 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A single traumatic brain injury is associated with an increased risk of dementia and, in a proportion of patients surviving a year or more from injury, the development of hallmark Alzheimer's disease-like pathologies. 4 key findings →
Design: longitudinal study Participants: 52 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Of 4467 participants who underwent 9208 longitudinal cognitive sessions, 2698 (60.4%) were female, and the mean age (SD) was 74.3 (9.2) years; 3213 were cognitively unimpaired, 972 had mild cognitive impairment, and 282 had AD dementia. 2 key findings →
Design: cohort study Participants: 4,467 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These data suggest that resveratrol decreases CSF MMP9, modulates neuro-inflammation, and induces adaptive immunity. 3 key findings →
Participants: 119 Evidence: low
Full summary, score breakdown and related studies → Original source
Among the individual plasma p-tau variants, p-tau217 consistently outperformed p-tau181 and p-tau231. 4 key findings →
Design: longitudinal study Participants: 352 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cognition ranged from high to early cognitive decline (median Mini-Mental State Examination [MMSE] score = 26). 5 key findings →
Design: longitudinal study Participants: 60 Evidence: moderate
Full summary, score breakdown and related studies → Original source
First, we mapped SVs across 81 AD risk loci and discovered 22 SVs in linkage disequilibrium (LD) with GWAS lead variants and directly associated with the phenotypes tested. 5 key findings →
Design: cohort study Participants: 1,088 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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
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.
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 31,780 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 31,780 records, built mostly from automated pulls of Europe PMC (66% of the library) and OpenAlex (16%), 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.
1,052 records (3.3% of the library) are not peer-reviewed — 973 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 →
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