79/100
✓ Peer-reviewed
alzhub usefulness score 79 out of 100.
·
Brain
·
2025-02-03
Plasma %p-tau217WashU had the highest performance, with significantly higher AUCs than all the immunoassays (Pdiff < 0.007). 5 key findings →
Design: cohort
Participants: 998
Evidence: high
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We found a sequence to pathological changes, with rates of Aβ deposition in mutation carriers being significantly different from those in non-carriers first (across regions that showed a significant difference, at a mean of 18·9 years [SD 3·3] before expected onset), followed by hypometabolism (14·1 years [5·1] before expected onset), and lastly structural decline (4·7 years [4·2] before expected onset). 2 key findings →
Design: longitudinal study
Participants: 346
Evidence: moderate
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76/100
✓ Peer-reviewed
alzhub usefulness score 76 out of 100.
·
JAMA Neurology
·
2024-09-01
In BioFINDER-2, the mean (SD) age was 65.7 (14.4) with 261 females (52.7%). 3 key findings →
Design: cohort
Participants: 983
Evidence: moderate
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76/100
✓ Peer-reviewed
alzhub usefulness score 76 out of 100.
·
JAMA network open
·
2025-03-03
Age, sex, and apolipoprotein E (APOE) are the strongest risk factors for late-onset Alzheimer disease (AD). 4 key findings →
Design: meta-analysis
Participants: 4,592
Evidence: high
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Amyloid-beta 42 (Aβ42) and phosphorylated tau (pTau) levels in cerebrospinal fluid (CSF) reflect core features of the pathogenesis of Alzheimer's disease (AD) more directly than clinical diagnosis. 2 key findings →
Participants: 8,074
Evidence: low
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In this prospective cohort study, we included adults aged 40 years or older with subjective cognitive decline, mild cognitive impairment, or dementia, based on cognitive test results and clinical assessments, consecutively recruited at two memory clinics in Sweden, as part of the Swedish BioFINDER-2 study. 3 key findings →
Design: cohort
Participants: 572
Evidence: high
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Coding variants in the triggering receptor expressed on myeloid cells 2 (TREM2) are associated with late-onset Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study
Evidence: moderate
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70/100
✓ Peer-reviewed
alzhub usefulness score 70 out of 100.
·
Nature medicine
·
2026-02-19
Predicting not just if, but also when, cognitively unimpaired individuals are likely to develop onset of Alzheimer's disease (AD) symptoms would be useful to clinical trials and, eventually, clinical practice. 2 key findings →
Design: cohort
Participants: 603
Evidence: moderate
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Low frequency coding variants in TREM2 are associated with increased Alzheimer disease (AD) risk, while loss of functions mutations in the gene lead to an autosomal recessive early-onset dementia, named Nasu-Hakola disease (NHD). 5 key findings →
Design: case-control study
Participants: 180
Evidence: moderate
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TREM2 is a transmembrane receptor that is predominantly expressed by microglia in the central nervous system. 4 key findings →
Design: cross-sectional
Participants: 1,027
Evidence: moderate
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TREM and TREM-like receptors are a structurally similar protein family encoded by genes clustered on chromosome 6p21.11. 4 key findings →
Design: meta-analysis
Evidence: high
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68/100
✓ Peer-reviewed
alzhub usefulness score 68 out of 100.
·
JAMA Neurology
·
2026-07-01
The BioFINDER-2 main cohort included 872 participants, with an additional 156 participants in the Knight ADRC cohort for independent validation. 2 key findings →
Design: cohort
Participants: 1,028
Evidence: high
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68/100
✓ Peer-reviewed
alzhub usefulness score 68 out of 100.
·
Nature genetics
·
2022-11-21
Alzheimer's disease (AD), the leading cause of dementia, has an estimated heritability of approximately 70% 1 . 3 key findings →
Participants: 32,558
Evidence: low
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67/100
✓ Peer-reviewed
alzhub usefulness score 67 out of 100.
·
Nature medicine
·
2023-07-13
Aggregated insoluble tau is one of two defining features of Alzheimer's disease. 3 key findings →
Participants: 448
Evidence: low
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67/100
✓ Peer-reviewed
alzhub usefulness score 67 out of 100.
·
Neurology
·
2021-12-14
Plasma Aβ42/Aβ40 is a robust measure for detecting amyloid plaques and can be utilized to aid in the diagnosis of AD, identify those at risk for future dementia due to AD, and improve the diversity of populations enrolled in AD research and clinical trials. 3 key findings →
Participants: 465
Evidence: moderate
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Across the brain, people with Down syndrome had greater concentrations of tau for a given level of amyloid compared with people with autosomal-dominant Alzheimer's disease. 3 key findings →
Design: cohort study
Participants: 137
Evidence: moderate
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67/100
✓ Peer-reviewed
alzhub usefulness score 67 out of 100.
·
JAMA neurology
·
2013-05-01
Sleep and circadian problems are very common in Alzheimer disease (AD). 4 key findings →
Design: cross-sectional
Participants: 145
Evidence: moderate
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67/100
✓ Peer-reviewed
alzhub usefulness score 67 out of 100.
·
Nature Medicine
·
2025-03-31
Insoluble tau aggregates within neurofibrillary tangles are a defining neuropathological feature of Alzheimer’s disease (AD) and closely correlate with clinical symptoms. 2 key findings →
Participants: 108
Evidence: low
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66/100
✓ Peer-reviewed
alzhub usefulness score 66 out of 100.
·
Nature medicine
·
2020-01-13
Glia have been implicated in Alzheimer's disease (AD) pathogenesis. 4 key findings →
Evidence: low
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65/100
✓ Peer-reviewed
alzhub usefulness score 65 out of 100.
·
Nature
·
2017-09-20
APOE4 is the strongest genetic risk factor for late-onset Alzheimer disease. 5 key findings →
Evidence: low
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We found that longitudinal changes in cognitive function measured by the cognitive composite decreased at low and high values of total sleep time (P < 0.001), time in non-REM (P < 0.001) and REM sleep (P < 0.001), sleep efficiency (P < 0.01) and <1 Hz and 1-4.5 Hz non-REM slow wave activity (P < 0.001) even after adjusting for age, CSF total tau/amyloid-β42 ratio, APOE ε4 carrier status, years of education and sex. 2 key findings →
Design: cross-sectional
Participants: 100
Evidence: moderate
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65/100
✓ Peer-reviewed
alzhub usefulness score 65 out of 100.
·
JAMA neurology
·
2015-11-01
Baseline CSF levels of NGRN in patients with AD (median level, 2381 pg/mL [interquartile range, 1651-3416 pg/mL]) were higher than in cognitively normal participants (median level, 1712 pg/mL [interquartile range, 1206-2724 pg/mL]) (P = .04). 3 key findings →
Design: longitudinal study
Participants: 163
Evidence: moderate
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64/100
✓ Peer-reviewed
alzhub usefulness score 64 out of 100.
·
Neurology
·
2013-04-10
Abnormal levels of all biomarkers were associated with faster time to cognitive impairment, and some participants with abnormal biomarker levels remained cognitively normal for up to 6.6 years. 2 key findings →
Design: longitudinal study
Participants: 201
Evidence: moderate
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CSF Aβ42 levels are tightly coupled with cortical amyloid load in the earliest stages of preclinical AD, and begin to decrease dramatically prior to the point when an abnormal threshold of cortical accumulation is detected with amyloid imaging. 1 key finding →
Design: longitudinal study
Participants: 164
Evidence: moderate
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64/100
✓ Peer-reviewed
alzhub usefulness score 64 out of 100.
·
JAMA neurology
·
2016-10-01
Among the 174 participants (81 men [46.6%]; 93 women [53.4%]; mean [SD] age, 65.7 [8.9] years), a proportion (14%-17%) of individuals with neurodegeneration alone (SNAP) later demonstrated Aβ+. 1 key finding →
Design: cohort study
Participants: 174
Evidence: moderate
Full summary, score breakdown and related studies →
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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.