27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
BackgroundAlzheimer's disease (AD) accounts for the majority of dementia-related disorders among aging populations. 2 key findings →
Design: systematic review Evidence: high
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Low baseline Aβ42/Aβ40 was significantly associated with increased amyloid accumulation (β = 0.257, 95% confidence interval (CI) 0.177-0.336, P < 0.001), and with higher risk of conversion to Aβ-PET positivity (Hazard ratio (HR) = 2.84, 95% CI 1.14-7.04, P = 0.025) and to MCI due to AD (HR = 3.25, 95% CI 1.17-9.01, P = 0.024). 5 key findings →
Design: longitudinal study Participants: 200 Evidence: moderate
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Neuropsychiatric symptoms (NPS), commonly concomitant with Alzheimer's disease (AD), substantially impair the quality of life and accelerate disease progression, yet reliable biomarkers for early identification of individuals at high NPS risk remain elusive. 4 key findings →
Design: longitudinal study Participants: 509 Evidence: moderate
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Eight studies comprising 984 patients met inclusion criteria. 5 key findings →
Design: systematic review Participants: 984 Evidence: high
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P-tau217 demonstrated the most significant inter-group differences, the highest hazard ratio, and best distinguished MCI-Converters from MCI-Nonconverters, with its discriminative performance comparable to that of Aβ-PET measures and multi-plasma biomarker models. 5 key findings →
Design: longitudinal study Participants: 47 Evidence: moderate
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Parkinson's disease (PD) is a neurodegenerative condition that may affect both motor and cognitive function. 1 key finding →
Design: longitudinal study Participants: 115 Evidence: moderate
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Most dementias are preceded by mild cognitive impairment (MCI), a transitional clinical stage characterized by cognitive decline that does not yet significantly interfere with activities of daily living. 5 key findings →
Design: systematic review Evidence: high
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Accurate prediction of progression from mild cognitive impairment (MCI) to Alzheimer's disease (AD) is critical for early intervention. 1 key finding →
Design: longitudinal study Participants: 596 Evidence: moderate
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The prominent prognostic role of carotid plaques in Aβ-negative MCI underscores the vascular contributions to non-amyloid cognitive decline and highlights the importance of evaluating both AD-related and vascular mechanisms in prodromal dementia. 1 key finding →
Design: longitudinal study Participants: 58 Evidence: moderate
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The prevalence of PIMcogs increased from 16% at baseline to 23% at follow-up. 5 key findings →
Participants: 397 Evidence: low
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Disruptions in GABAergic activity and alterations in gamma oscillations are key pathological features of AD associated with amyloid-beta (Aβ) plaques. 3 key findings →
Design: longitudinal study Participants: 127 Evidence: moderate
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We identified 8 brain structural features from 192 MRI features that were associated with the risk of MCI progressing to AD, including: left hippocampus, left inferior lateral ventricle, left amygdala, right middle temporal gyrus, left fusiform gyrus, right amygdala, left cortical total volume, and brain parenchyma total volume. 4 key findings →
Design: longitudinal study Participants: 947 Evidence: moderate
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In amyloid PET–positive MCI, Ginkgo biloba use was associated with sustained clinical stability, reduced plasma Aβ oligomerization tendency, and attenuation of amyloid PET progression over 18 months. 2 key findings →
Design: cohort study Participants: 21 Evidence: moderate
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Subjective cognitive decline (SCD) is increasingly recognised as a potential preclinical stage of Alzheimer's disease, yet the physiological mechanisms underlying its progression remain poorly understood. 4 key findings →
Design: longitudinal study Evidence: moderate
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Alzheimer's disease (AD) develops over a prolonged asymptomatic phase marked by silent pathology. 1 key finding →
Participants: 102 Evidence: low
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Dementia developed in 104 individuals (29.6%), including 85 (22.4%) who met core clinical criteria for probable and possible Alzheimer's disease dementia. 3 key findings →
Participants: 398 Evidence: low
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Mild cognitive impairment (MCI) is an early stage in the progression toward dementia. 1 key finding →
Design: longitudinal study Evidence: moderate
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This study highlights the role of age, gender, APOE genotype, and depressive symptoms in the presentation and progression of cognitive decline. 2 key findings →
Evidence: moderate
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EEG/ERP analysis suggested differences in frontal alpha asymmetry, power ratio, and ERP components between the MCI and CN groups. 5 key findings →
Participants: 70 Evidence: low
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Blood-based biomarkers (BBMs) for Alzheimer disease (AD) offer widely expanded access to biomarker-informed diagnoses in community settings that have previously lacked such resources. 1 key finding →
Evidence: low
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Event-related potentials (ERPs), particularly the P200 component, have been studied as potential biomarkers, but conventional grand-averaged approaches often yield inconsistent results. 5 key findings →
Participants: 636 Evidence: moderate
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Multicomponent and transdisciplinary interventions focused on the family member–patient dyad have the potential to optimize cognitive outcomes and quality of life. 1 key finding →
Participants: 40 Evidence: high
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SCD participants were older, had fewer years of education, more depressive symptoms, and more subjective cognitive complaints than CU participants. 4 key findings →
Participants: 315 Evidence: low
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The development of non-pharmacological treatment approaches is supported by evidence that addressing key modifiable risk factors may prevent or delay up to 45% of dementia cases. 5 key findings →
Evidence: low
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We found interactions between APOE4 and cognitive states in the aperiodic EEG exponent and the spectral power ratio (SPR). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 →