Bapineuzumab did not improve clinical outcomes in patients with Alzheimer's disease, despite treatment differences in biomarkers observed in APOE ε4 carriers. 1 key finding →
Design: clinical trial
Participants: 1,090
Evidence: high
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Homozygous loss-of-function mutations in TREM2, encoding the triggering receptor expressed on myeloid cells 2 protein, have previously been associated with an autosomal recessive form of early-onset dementia. 4 key findings →
Design: meta-analysis
Participants: 1,092
Evidence: high
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The drug did not prevent clinical progression in a trial involving patients with mild-to-moderate dementia due to Alzheimer's disease. 4 key findings →
Participants: 1,454
Evidence: high
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Verubecestat did not reduce cognitive or functional decline in patients with mild-to-moderate Alzheimer's disease and was associated with treatment-related adverse events. 3 key findings →
Participants: 1,958
Evidence: high
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Alzheimer's disease is characterized by amyloid-beta (Aβ) plaques and neurofibrillary tangles. 4 key findings →
Design: clinical trial
Participants: 2,129
Evidence: low
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After a median of 4.7 years of follow-up, the rate of cardiovascular disease was 10.7 events per 1000 person-years in the aspirin group and 11.3 events per 1000 person-years in the placebo group (hazard ratio, 0.95; 95% confidence interval [CI], 0.83 to 1.08). 4 key findings →
Participants: 19,114
Evidence: low
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Among persons with early Alzheimer's disease, the use of gantenerumab led to a lower amyloid plaque burden than placebo at 116 weeks but was not associated with slower clinical decline. 2 key findings →
Design: clinical trial
Participants: 980
Evidence: low
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The mean CDR-SB score at baseline was approximately 3.2 in both groups. 2 key findings →
Design: clinical trial
Participants: 1,795
Evidence: low
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In patients with early Alzheimer's disease, donanemab resulted in a better composite score for cognition and for the ability to perform activities of daily living than placebo at 76 weeks, although results for secondary outcomes were mixed. 3 key findings →
Design: clinical trial
Participants: 257
Evidence: low
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Solanezumab, which targets monomeric amyloid in persons with elevated brain amyloid levels, did not slow cognitive decline as compared with placebo over a period of 240 weeks in persons with preclinical Alzheimer's disease. 3 key findings →
Design: clinical trial
Participants: 1,169
Evidence: low
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Higher all-cause mortality was observed among apparently healthy older adults who received daily aspirin than among those who received placebo and was attributed primarily to cancer-related death. 3 key findings →
Participants: 19,114
Evidence: low
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Dementia represents a substantial financial burden on society, one that is similar to the financial burden of heart disease and cancer. 3 key findings →
Design: longitudinal study
Participants: 856
Evidence: moderate
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The outcomes were better among patients treated with rivastigmine than among those who received placebo; however, the differences between these two groups were moderate and similar to those reported in trials of rivastigmine for Alzheimer's disease. 3 key findings →
Participants: 541
Evidence: low
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The long-term use of NSAIDs may protect against Alzheimer's disease but not against vascular dementia. 3 key findings →
Design: cohort study
Participants: 6,989
Evidence: moderate
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Sequence variants, including the ε4 allele of apolipoprotein E, have been associated with the risk of the common late-onset form of Alzheimer's disease. 4 key findings →
Design: case-control study
Evidence: moderate
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In this 12-week trial, donepezil was not more effective than placebo in treating agitation in patients with Alzheimer's disease. 3 key findings →
Participants: 272
Evidence: low
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The disclosure of APOE genotyping results to adult children of patients with Alzheimer's disease did not result in significant short-term psychological risks. 5 key findings →
Evidence: high
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However, the advisory did not apply to conventional antipsychotic medications; the risk of death with these older agents is not known. 1 key finding →
Design: cohort study
Participants: 22,890
Evidence: moderate
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Participation in leisure activities is associated with a reduced risk of dementia, even after adjustment for base-line cognitive status and after the exclusion of subjects with possible preclinical dementia. 5 key findings →
Design: prospective cohort
Participants: 469
Evidence: moderate
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We treated 17 patients who had moderate to severe Alzheimer's disease with oral tetrahydroaminoacridine (THA), a centrally active anticholinesterase, in a three-phase study. 3 key findings →
Participants: 17
Evidence: low
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The APOE epsilon4 allele is associated with the risk of late-onset Alzheimer's disease. 4 key findings →
Design: longitudinal study
Participants: 815
Evidence: moderate
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Among participants in the Framingham Heart Study, the incidence of dementia has declined over the course of three decades. 3 key findings →
Participants: 5,205
Evidence: low
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An increased plasma homocysteine level is a strong, independent risk factor for the development of dementia and Alzheimer's disease. 3 key findings →
Design: cross-sectional
Participants: 1,092
Evidence: low
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Vitamin E had no benefit in patients with mild cognitive impairment. 5 key findings →
Participants: 769
Evidence: low
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In this study involving Chinese participants during the 20 years preceding clinical diagnosis of sporadic Alzheimer's disease, we observed the time courses of CSF biomarkers, the times before diagnosis at which they diverged from the biomarkers from a matched group of participants who remained cognitively normal, and the temporal order in which the biomarkers became abnormal. 2 key findings →
Design: case-control study
Participants: 648
Evidence: moderate
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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
- Randomized / 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
- Multicenter 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 31,380 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.