Type 2 diabetes is associated with hippocampal and amygdalar atrophy, regardless of vascular pathology. 4 key findings →
Participants: 506 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Type 2 diabetes is associated with hippocampal and amygdalar atrophy, regardless of vascular pathology. 4 key findings →
Participants: 506 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebral microbleeds might indicate a higher risk of future intracerebral hemorrhage and may be a marker of cerebral small-vessel disease and cerebral amyloid angiopathy. 4 key findings →
Participants: 5,200 Evidence: low
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Tau PET imaging with (18)F-AV-1451 could serve as an in vivo biomarker for the evaluation of AD-related tau pathology and monitoring disease progression. 2 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Doubly dissociated areas of hypoperfusion in FTLD and AD are consistent with areas of significant histopathologic burden in these groups. 5 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Vascular disease in the brain is prevalent among incident dementia cases. 1 key finding →
Participants: 3,375 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Different patterns of gray matter density distribution in patients with mild cognitive impairment may be associated to different rates of conversion to Alzheimer disease. 3 key findings →
Participants: 22 Evidence: low
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Heart failure is a risk factor for Alzheimer's disease and cerebrovascular disease. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These findings suggest that at current expected prices, neither aducanumab nor donanemab would be cost-effective for early AD in the US. 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The targeted brain dysfunction that accompanies aging can have a devastating effect on cognitive and intellectual abilities. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our study supports the usefulness of [ 18 F]AV1451 to characterize tau pathology in at least a subset of pathogenic MAPT mutations. 5 key findings →
Evidence: low
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Low serum albumin may increase the risk of AD dementia by elevating amyloid accumulation. 2 key findings →
Participants: 396 Evidence: low
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Concluding, this innovative EEG analysis, in combination with a genetic test (both low-cost and widely available), could evaluate on an individual basis with great precision the risk of MCI progression. 3 key findings →
Participants: 97 Evidence: low
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Our study showed an association between neurofibrillary pathology and frontal PVWMH and DWMH (rather than parietal), as a surrogate of small vessel disease, particularly in very old community-dwelling individuals. 5 key findings →
Participants: 132 Evidence: moderate
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Percent total HSI, ventricular, and total CSF volume measures can independently predict the rate of cognitive decline and improve the predictive power of statistical models that use only clinical data. 4 key findings →
Design: longitudinal study Evidence: moderate
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Our proof-of-concept study is the first to show that microstructural and macrostructural changes can reflect underlying neuroinflammatory mechanisms in early stages of Alzheimer disease (AD). 2 key findings →
Participants: 31 Evidence: low
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Studies of autosomal dominant Alzheimer disease (AD) have shown structural and cognitive changes in mutation carriers decades prior to clinical disease. 1 key finding →
Participants: 717 Evidence: moderate
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Microglial activation distributes preferentially along highly connected brain regions, similar to tau pathology. 5 key findings →
Participants: 32 Evidence: low
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Baseline 18F-MK-6240 PET showed a minimal signal in CU participants, localized signal to the medial temporal lobe in participants with MCI, and a signal spanning the inferolateral temporal lobe and extending posteriorly along the ventral cortex in participants with AD. 5 key findings →
Design: longitudinal study Participants: 27 Evidence: moderate
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Amyloid deposition can be identified among cognitively normal elderly persons during life, and the prevalence of asymptomatic amyloid deposition may be similar to that of symptomatic amyloid deposition.
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Our study demonstrated the robustness of a multisite Centiloid [ 11 C]PIB‐PET study and established a range of pathology‐based CL thresholds.
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Apraxia of speech is a motor speech disorder characterized by combinations of slow speaking rate, abnormal prosody, distorted sound substitutions, and trial-and-error articulatory movements. 1 key finding →
Design: cross-sectional Participants: 14 Evidence: low
Full summary, score breakdown and related studies → Original source
18 F-MK-6240 recapitulated Braak staging and correlated with CSF tau and p-tau, normalized to Aβ42 . 18 F-MK-6240 negatively correlated with age across Braak regions in amyloid-positive participants, consistent with greater tau pathology in earlier onset AD. 2 key findings →
Participants: 101 Evidence: low
Full summary, score breakdown and related studies → Original source
In both cohorts, we observed that tau-PET standardized uptake value ratio in medial temporal lobes was associated with clinical dementia rating Sum of Boxes (CDR-SoB) scores independently of local amyloid-PET uptake (FWE corrected at p < 0.001). 5 key findings →
Participants: 154 Evidence: moderate
Full summary, score breakdown and related studies → Original source
GMM-based cutoffs classified less subjects as T+, mainly in the A- CN (<3.4% vs >28.5%) and A+ CN (<14.5% vs >42.9%) groups and showed higher agreement with visual rating (ICC=0.91 vs ICC<0.62) than published cutoffs. 3 key findings →
Participants: 269 Evidence: low
Full summary, score breakdown and related studies → Original source
A subset of participants received cognitive testing and/or the Movement Disorders Society Unified Parkinson's Disease Rating Scale Part III motor exam (off medication). 18F-PI-2620 uptake was low overall in Lewy body disease and correlated with β-amyloid PET in temporal lobe regions and precuneus. 5 key findings →
Participants: 29 Evidence: low
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 →