Seizures in people with dementia (PWD) are associated with faster cognitive decline and worse clinical outcomes. 3 key findings →
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.
Seizures in people with dementia (PWD) are associated with faster cognitive decline and worse clinical outcomes. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
See Vandenberghe and Schaeverbeke (doi:10.1093/awx065) for a scientific commentary on this article. 3 key findings →
Design: cross-sectional Evidence: moderate
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Beta-amyloid (Abeta) deposition is pathognomic for Alzheimer's disease (AD), but may occur in normal elderly people without apparent cognitive effect.
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Hyperphosphorylated tau protein (P-tau) in CSF is a core biomarker candidate of Alzheimer's disease.
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Beta amyloid is one of the major histopathological hallmarks of Alzheimer's disease.
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We found a wide range of behavioural changes across FTD. 5 key findings →
Evidence: low
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Model scores two standard deviations below the mean had 4 months increased survival (two standard deviations below had 3 months decreased survival). 5 key findings →
Participants: 802 Evidence: low
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Neurodegeneration in Parkinson's disease dementia (PDD) and dementia with Lewy bodies (DLB) affect cortical and subcortical networks involved in saccade generation. 5 key findings →
Participants: 20 Evidence: low
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Dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD) are subtypes of Lewy body dementia, and are considered two ends of a disease spectrum. 5 key findings →
Participants: 66 Evidence: low
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Recent advancements in computational approaches and neuroimaging techniques have refined our understanding of the precuneus. 3 key findings →
Evidence: low
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Genome-wide association studies have identified a number of risk variants for Alzheimer’s disease implicated in inflammatory responses (Bettens et al., 2013); exome sequencing has revealed polymorphisms in the microglial receptor TREM2 gene as a rare but significant risk for Alzheimer’s disease (Guerreiro et al., 2013; Jonsson et al., 2013); and recently, the CD33 risk allele has been shown to inhibit microglial clearance of amyloid-β (Bradshaw et al., 2013; Griciuc et al., 2013). 5 key findings →
Participants: 39 Evidence: low
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These same brain areas were then assessed in a cohort of patients with Alzheimer’s disease versus a healthy older reference group, using a region of interest approach combined with standard structural (MRI), metabolic (fluorodeoxyglucose-PET) and amyloid ligand (florbetapir-PET) neuroimaging. 5 key findings →
Evidence: moderate
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An alternative model, the multiple trace theory (MTT), suggests that the capacity of the MTL to recollect episodic memories is of a more permanent nature. 2 key findings →
Participants: 13 Evidence: low
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This molecular genetics study found that several TREM2 gene variants previously thought to work only by altering the TREM2 protein itself, also disrupt how the TREM2 gene's RNA message is spliced together, sometimes producing dysfunctional protein versions. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our findings were compared to other published RNA sequencing data of tauopathies (Alzheimer's dementia, progressive supranuclear palsy and FTLD with MAPT), FTLD-TDP (subtypes A&B) and available proteomics of this cohort. 5 key findings →
Evidence: moderate
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Ninety per cent of the human population has been right-handed since the Paleolithic, yet the brain signature and genetic basis of handedness remain poorly characterized. 5 key findings →
Evidence: low
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As more biomarkers for Alzheimer's disease and age-related brain conditions become available, more sophisticated analytic approaches are needed to take full advantage of the information they convey. 2 key findings →
Evidence: low
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We present the pharmacological properties of EKZ-438, which demonstrate high selectivity for HDAC6 (>8500-fold selectivity for HDAC6 versus all other HDAC6 paralogues), low nanomolar potency (12 nM) for HDAC6, and importantly, CNS-penetrance (unbound brain-to-plasma partition coefficient [Kp,uu,brain] ≥ 0.55) and high oral bioavailability (fraction of dose absorbed [F%] = 70). 3 key findings →
Evidence: low
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Here, we show that cofilin is hyper-phosphorylated in human ALS and disease models compared to controls. 4 key findings →
Evidence: low
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Pathological aggregation of tau is a hallmark of Alzheimer’s disease and related tauopathies. 3 key findings →
Evidence: low
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While neuropathological and genetic studies have established the crucial involvement of TDP-43 proteinopathy in the pathogenesis of amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and related neurodegenerative disorders, multiple studies have described the presence of TDP-43 inclusions in muscular disorders, including inclusion body myositis but also other related rimmed vacuole myopathies. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Although the patterns of structural and metabolic brain alterations in Alzheimer's disease are being refined and discrepancies between them are being underlined, the exact relationships between atrophy and hypometabolism are still unclear. 3 key findings →
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 →