28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
MpHE efficiently reduced astrogliosis, the presence of insoluble Aβ peptides in the hippocampus and spatial learning impairments, of both, lean, and obese 5XFAD mice. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Redistribution of the water channel aquaporin-4 (AQP4) away from astrocyte endfeet and into parenchymal processes is a striking histological feature in mouse models of Alzheimer's disease (AD) and other neurological conditions with prominent astrogliosis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Traumatic brain injuries (TBI) are an important public health challenge. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study was designed to explore the influence of apolipoprotein E (APOE) on blood phospholipids (PL) in predicting preclinical Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
CSF can be stored for up to 72 h at RT, 1 week at 4 °C, or at least 2 weeks at either - 20 °C or - 80 °C before Aβ measurements. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study demonstrates that deep cervical LVA is safe and feasible procedure, showing a significant cognitive improvement in AD patients (mainly in MMSE), which needs long-term follow-up and large-scale clinical trials to verify. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The Leu85Pro mutation in PSEN1 was pathogenic. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genetic variations play an important role in the clinical presentation and progression of Alzheimer's disease (AD), especially early-onset Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Missense mutations in presenilin 1 cause early onset familial Alzheimer's disease in a way that is not understood. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Early-onset dominantly inherited forms of Alzheimer's disease (AD) are rare, but studies of such cases have revealed important information about the disease mechanisms. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We demonstrate that targeted inhibition of the PS1-Syt1 binding in neurons, without changing the proteins' expression level, triggers "pathogenic" conformational shift of PS1, and consequent increase in the Aβ42/40 ratio. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
To evaluate whether the polygenic profile modifies the development of sporadic Alzheimer's disease (sAD) and pathological biomarkers in cerebrospinal fluid (CSF), 462 sAD patients and 463 age-matched cognitively normal (CN) controls were genotyped for 35 single-nucleotide polymorphisms (SNPs) that are significantly associated with sAD. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
One of the hallmarks of Alzheimer's disease is the formation of extracellular amyloid plaques that consist mainly of abnormally aggregated forms of amyloid β (Aβ) peptides. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuropathological investigations report that in synucleinopathies with dementia, namely Parkinson's disease (PD) with dementia (PDD) and dementia with Lewy bodies (DLB), the histopathological hallmarks of Alzheimer's Disease (AD), in particular amyloid plaques, are frequently observed. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
TSA induced a remarkable amelioration of learning and memory impairments in APPswe/PS1dE9 mice through the regulation of Aβ42, Aβ40, carbohydrate and vitamin metabolites in the hippocampus and LDL-C and CHOL in the plasma. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our results suggest that the mechanism underlying low CSF Aβ levels differs between amyloid PET(-) iNPH and amyloid PET(+) AD subjects. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings using DTI-ALPS method found a positive correlation between cognitive decline and GS dysfunction in LOE patients, and may indicate a potential internal link between age-related LOEU and dementia formation. 5 key findings →
Design: post-hoc analysis Evidence: low
Full summary, score breakdown and related studies → Original source
The possible pathogenic nature of the mutation is not clarified. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a severe neurodegenerative disease that requires early diagnosis to manage its progression. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Detection of amyloid-β (Aβ) aggregates contributes to the diagnosis of Alzheimer disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cognitive deficits exhibited by FAD rats were not exacerbated by the introduction of the SHRSP phenotype, nor was the hyperactivity phenotype associated with SHRSP altered by the FAD transgene. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's Disease (AD) is the most common form of dementia, characterised by extracellular amyloid deposition as plaques and intracellular neurofibrillary tangles of tau protein. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These results indicated that a range of disease specific TDP-43 variants are generated in ALS patients with different variants being generated in sporadic and familial cases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This nanostructured conductive interface favors penetration of water-soluble biomolecules and catalyzes a redox reaction, providing limits of detection (LOD) of 6.63 pg/mL for Aβ 40 and 3.74 pg/mL for Aβ 42 . 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Among mediators of inflammation, chemokines play a pivotal role in the neuroinflammatory process related to Alzheimer's disease (AD). 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.
1,034 records (3.7% 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 →