27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
NfL in both serum and CSF has the potential to serve as a biomarker for clinical disease onset and has a prognostic value in genetic FTD. 1 key finding →
Design: case-control study Participants: 174 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Patients with behavioural Alzheimer's disease showed worse memory scores than behavioural variant frontotemporal dementia and did not differ from typical Alzheimer's disease, while executive function composite scores were lower compared to behavioural variant frontotemporal dementia and typical Alzheimer's disease. 3 key findings →
Participants: 17 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Since its opening in 2000, patient care and research go hand in hand at the Alzheimer center of the VU University Medical Center, both organized in such a way that they mutually strengthen each other. 1 key finding →
Participants: 4,000 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Baseline CSF was collected from 512 patients with Alzheimer disease (AD) and 272 patients with other types of dementia (OD), 135 patients with a psychiatric disorder (PSY), and 275 patients with subjective memory complaints (SMC). 4 key findings →
Participants: 512 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The extent to which specific factors influence diagnostic delays in dementia is unclear. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Frontotemporal dementia (FTD) is the second most common young-onset dementia and is clinically characterised by progressive behavioural change, executive dysfunction and language difficulties. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the most common cause of dementia at older age. 2 key findings →
Participants: 270 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Low Aβ42 was the strongest predictor of clinical progression in patients with subjective complaints. 3 key findings →
Participants: 127 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Frontotemporal dementia (FTD) is a pathologically heterogeneous group of presenile neurodegenerative disorders, with or without the deposition of hyperphosphorylated tau protein in affected brain regions. 4 key findings →
Design: case-control study Participants: 18 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
[(11)C]PIB scans were positive in 40 of 66 (61%) patients with a clinical diagnosis of Alzheimer's disease (AD), 5 of 18 (28%) patients with frontotemporal dementia (FTD), 4 of 5 (80%) patients with Lewy body dementia, and 3 of 10 (30%) patients with other dementias. [(18)F]FDG uptake patterns matched the clinical diagnosis in 38 of 66 (58%) of AD patients, and in 6 of 18 (33%) FTD patients. 4 key findings →
Participants: 39 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
CSF biomarkers amyloid beta 1-42 (Abeta(42)), total tau (tau), and tau phosphorylated at threonine 181 (p-tau-181) are useful diagnostic markers for Alzheimer disease (AD). 4 key findings →
Participants: 151 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
CSF p/t-tau ratio and NfL levels are strongly driven by ALS status. 1 key finding →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source
The SVM can be used in single-subject discrimination and can help the clinician arrive at a diagnosis. 4 key findings →
Participants: 115 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) in younger patients is associated with a higher prevalence of atypical symptoms. 4 key findings →
Participants: 172 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer's disease is characterized both by a lower mean level of functional connectivity as well as by diminished fluctuations in the level of synchronization. 2 key findings →
Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
CSF Abeta42 was significantly lower and CSF total tau and CSF Ptau-181 significantly higher in EAD patients than FTLD patients and control subjects. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
With decreasing local and global connectivity parameters, the large-scale functional brain network organization in AD deviates from the optimal 'small-world' network structure towards a more 'random' type. 5 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source
Hippocampal atrophy is not only a characteristic of Alzheimer's disease but also occurs in FTLD. 5 key findings →
Participants: 42 Evidence: low
Full summary, score breakdown and related studies → Original source
In the diagnostic workup of relatively young dementia patients, CSF NFL levels may play a role in the discrimination between FTLD and EAD, especially in combination with Abeta42 and p-tau181 analysis. 2 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 →