27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
The NfL level was increased at baseline in patients with mild cognitive impairment and AD dementia (mean levels: cognitive unimpairment, 32.1 ng/L; mild cognitive impairment, 37.9 ng/L; and AD dementia, 45.9 ng/L; P Conclusions and relevance The findings suggest that plasma NfL can be used as a noninvasive biomarker associated with neurodegeneration in patients with AD and may be useful to monitor effects in trials of disease-modifying drugs. 3 key findings →
Design: cohort study Participants: 1,583 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
p75 neurotrophin receptor (p75 NTR ) signaling pathways substantially overlap with degenerative networks active in Alzheimer disease (AD). 2 key findings →
Participants: 242 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
We identified that combining plasma p-tau217 and a brief cognitive composite score was strongly related to greater risk of progression to AD dementia in MCI patients, suggesting that these measures could be key components of future prognostic algorithms for early AD. 2 key findings →
Participants: 110 Evidence: low
Full summary, score breakdown and related studies → Original source
Among 193 cognitively healthy controls, 197 patients with mild cognitive impairment, and 180 patients with AD with dementia, plasma NFL correlated with CSF NFL (Spearman ρ = 0.59, P Conclusions and relevance Plasma NFL is associated with AD diagnosis and with cognitive, biochemical, and imaging hallmarks of the disease. 3 key findings →
Design: case-control study Participants: 197 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Exclusion criteria included any significant neurologic disorder other than suspected AD; presence of infection, infarction, or multiple lacunes as detected by magnetic resonance imaging; and any significant systemic condition that could lead to difficulty complying with the protocol. 3 key findings →
Design: cohort study Participants: 1,113 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Inclusion criteria were early AD (mini-mental state examination [MMSE] score between 20 and 26 points or Alzheimer's disease assessment scale-cognitive subscale (ADAS-cog) score between 10 and 25 points), taking a stable dose of acetylcholinesterase inhibitor (donepezil, galantamine, or rivastigmine) for at least 4 months, a modified Hachinski score of 4 points or less, and CT or MRI results that were consistent with AD. 3 key findings →
Design: randomized controlled trial Participants: 78 Evidence: high
Full summary, score breakdown and related studies → Original source
No significant differences were found in the primary efficacy analysis. 2 key findings →
Design: clinical trial Participants: 234 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neuroinflammation and cerebrovascular dysfunction are early events occurring already at presymptomatic stages of AD and contribute to disease progression. 5 key findings →
Design: longitudinal study Participants: 508 Evidence: moderate
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The best CSF measures for identifying MCI-AD were Aβ42/total tau (t-tau) and Aβ42/hyperphosphorylated tau (p-tau) (area under the curve [AUC] 0.93-0.94). 3 key findings →
Design: longitudinal study Participants: 122 Evidence: moderate
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In response to sleep loss (+17.2%), compared with normal sleep (+1.8%), the evening to morning ratio was increased for t-tau ( p = 0.035). 4 key findings →
Evidence: high
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A combination of plasma phospho-tau (P-tau) and other accessible biomarkers might provide accurate prediction about the risk of developing Alzheimer's disease (AD) dementia. 2 key findings →
Participants: 340 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We evaluated the performance of CSF biomarkers for predicting risk of clinical decline and conversion to dementia in non-demented patients with cognitive symptoms. 4 key findings →
Design: longitudinal study Participants: 619 Evidence: moderate
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Emerging plasma biomarkers of Alzheimer's disease might be non-invasive tools to trace early Alzheimer's disease-related abnormalities such as the accumulation of amyloid-beta peptides, neurofibrillary tau tangles, glial activation and neurodegeneration. 4 key findings →
Design: longitudinal study Participants: 164 Evidence: moderate
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
Our results encourage an independent validation cohort study to confirm the indication that the plasma Aβ 1-40 /Aβ 1-42 ratio, assessed via Simoa, may improve future standard of care and clinical trial design. 2 key findings →
Design: cohort study Participants: 276 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Baseline plasma GFAP could detect abnormal CSF Aβ42/40 and CSF Aβ42/T-tau with an AUC of 0.79 (95% CI 0.72-0.86) and 0.80 (95% CI 0.72-0.86), respectively. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In a community-based cohort of 70-year olds, P-NfL was associated with both prevalent and incident CKD, while CSF and/or imaging measures did not differ by CKD status. 3 key findings →
Design: cohort study Participants: 744 Evidence: moderate
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Baseline biomarkers largely do not predict risk for developing ARIA-E. ARIA-E was associated with significant longitudinal changes in several biomarkers, with larger reductions in amyloid PET and CSF p-tau and t-tau concentrations, and paradoxically greater hippocampal volume reduction and ventricular enlargement, suggesting that ARIA-E in bapineuzumab-treated cases may be related to increased Aβ efflux from the brain and affecting downstream pathogenic processes. 4 key findings →
Design: longitudinal study Participants: 1,512 Evidence: moderate
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Cerebrospinal fluid biomarkers may be useful to monitor the effects of novel disease-modifying anti-Aβ drugs in clinical trials. 3 key findings →
Design: clinical trial Participants: 19 Evidence: high
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Blood-based biomarkers hold great promise to revolutionize the diagnostic and prognostic work-up of Alzheimer's disease (AD) in clinical practice. 5 key findings →
Design: longitudinal study Evidence: moderate
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Cerebrospinal fluid NFL concentration (median [interquartile range]) was higher in the AD dementia group (1479 [1134-1842] pg/mL), stable MCI group (no progression to AD during follow-up; 1182 [923-1687] pg/mL), and progressive MCI group (MCI with progression to AD dementia during follow-up; 1336 [1061-1693] pg/mL) compared with control participants (1047 [809-1265] pg/mL) (P Conclusions and relevance Cerebrospinal fluid NFL concentration is increased by the early clinical stage of AD and is associated with cognitive deterioration and structural brain changes over time. 2 key findings →
Design: longitudinal study Participants: 95 Evidence: moderate
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Plasma Aβ42/Aβ40${{\rm A}\beta }_{42}/{{\rm A}\beta }_{40}$ may begin declining decades prior to brain amyloid accumulation, whereas p-tau ratios, GFAP, and NfL increase closer in time. 1 key finding →
Design: longitudinal study Participants: 199 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) tau (total tau, T-tau), neurofilament light (NFL), and neurogranin (Ng) are potential biomarkers for neurodegeneration in Alzheimer's disease (AD). 3 key findings →
Design: longitudinal study Participants: 93 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 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.
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 →