Rates of cognitive decline in Alzheimer's disease (AD) are extremely heterogeneous. 1 key finding →
Design: case-control study Participants: 3,397 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Research
30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Neurofilament light chain (NfL) is a promising fluid biomarker of disease progression for various cerebral proteopathies. 2 key findings →
Design: cross-sectional Participants: 187 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
With the emergence of Alzheimer's disease (AD) disease-modifying therapies, identifying patients who could benefit from these treatments becomes critical. 1 key finding →
Participants: 1,422 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
Changes in β-amyloid (Aβ) and hyperphosphorylated tau (T) in brain and cerebrospinal fluid (CSF) precede Alzheimer's disease (AD) symptoms, making the CSF proteome a potential avenue to understand disease pathophysiology and facilitate reliable diagnostics and therapies. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The mean age was 74.2 years (SD, 8.3 years), 48% were women, 23% had subjective cognitive decline, 44% had mild cognitive impairment, and 33% had dementia. 2 key findings →
Participants: 307 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Higher eGFR was associated with increased levels of plasma p-tau217, p-tau181, Tau212-221, and Tau181-190 in individuals with cognitive impairment (cohort 1: R range, -0.24 to -0.59; P Conclusions and relevance In this study, CKD was associated with increased plasma levels of soluble tau, but for p-tau217 the associations were considerably lower than the association with Aβ positivity. 4 key findings →
Design: cross-sectional Participants: 141 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Biological staging of individuals with Alzheimer's disease (AD) may improve diagnostic and prognostic workup of dementia in clinical practice and the design of clinical trials. 4 key findings →
Design: longitudinal study Participants: 426 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Brain iron elevation is implicated in Alzheimer's disease (AD) pathogenesis, but the impact of iron on disease outcomes has not been previously explored in a longitudinal study. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
The very mildest symptomatic stage of AD exhibits the same CSF biomarker phenotype as more advanced AD. 1 key finding →
Design: longitudinal study Participants: 139 Evidence: moderate
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Within-person changes in CSF biomarkers were also compared with changes in cortical PiB binding and progression to a CDR higher than 0 at follow-up. 2 key findings →
Design: cohort study Participants: 169 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
65/100
The use of an amyloid clock enabled visualization and analysis of biomarker changes as a function of estimated years from symptom onset in sporadic AD. 1 key finding →
Design: cross-sectional Participants: 118 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
65/100
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
Full summary, score breakdown and related studies → Original source Free full text
The temporal evolutions and relative orderings of Alzheimer disease biomarkers, including CSF amyloid-β42 (Aβ42), Aβ40, total tau (Tau) and phosphorylated tau181 (pTau181), standardized uptake value ratio (SUVR) from the molecular imaging of cerebral fibrillar amyloid-β with PET using the 11C-Pittsburgh Compound-B (PiB), MRI-based hippocampal volume and cortical thickness and cognition have been hypothesized but not yet fully tested with longitudinal data for all major biomarker modalities among cognitively normal individuals across the adult lifespan starting from 18 years. 4 key findings →
Design: longitudinal study Participants: 2,609 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among cognitively normal participants with positive biomarkers, 34.4% developed cognitive impairment (Clinical Dementia Rating > 0) as compared to 8.4% of those with negative biomarkers. 2 key findings →
Design: longitudinal study Participants: 720 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
Studies evaluating the diagnostic test accuracy of plasma phosphorylated tau (p-tau) and amyloid beta (Aβ) tests (p-tau217, %p-tau217, p-tau181, p-tau231, and Aβ42/Aβ40) compared to reference standard tests (cerebrospinal fluid [CSF] AD biomarkers, amyloid positron emission tomography [PET], or neuropathology) in individuals with cognitive impairment (mild cognitive impairment or dementia) in specialized care settings were included. 4 key findings →
Design: meta-analysis Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We enrolled a cohort of 1070 PSEN1 E280A mutation carriers and 1074 non-carriers with baseline assessments; of these participants, longitudinal measures (with a mean follow-up of 6 years) were available for 242 mutation carriers and 262 non-carriers. 1 key finding →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Disease-modifying therapies for Alzheimer's disease (AD) are likely to be most beneficial when initiated in the presymptomatic phase. 2 key findings →
Design: cross-sectional Participants: 567 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
63/100
Using the Swedish BioFINDER-2 cohort [n = 1702, 50.7% male, mean (standard deviation) age 68.4 (12.2) years], we compared the associations between tau/Aβ-PET load and fluid biomarkers alone versus biomarkers in a ratio with a reference protein (Aβ40 or np-tau) in univariate linear regression models. 5 key findings →
Design: longitudinal study Participants: 1,702 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Anti-amyloid treatments for early symptomatic Alzheimer disease have recently become clinically available in some countries, which has greatly increased the need for biomarker confirmation of amyloid pathology. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a progressive neurodegenerative disease with a complex and heterogeneous pathophysiology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
With the aging US population and increasing incidence of Alzheimer disease (AD), understanding factors contributing to driving cessation among older adults is crucial for clinicians. 4 key findings →
Design: longitudinal study Participants: 283 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is characterized by two molecular pathologies: cerebral β-amyloidosis in the form of β-amyloid (Aβ) plaques and tauopathy in the form of neurofibrillary tangles, neuritic plaques, and neuropil threads. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events