The patterns of FDG decline are distinct in these 2 genetically determined forms of AD. 1 key finding →
Design: cross-sectional Participants: 76 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The patterns of FDG decline are distinct in these 2 genetically determined forms of AD. 1 key finding →
Design: cross-sectional Participants: 76 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
No amyloid-related imaging abnormalities occurred. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD), the most common cause of dementia in the elderly, is a complex neurodegenerative disease marked by the appearance of amyloid-β (Aβ) plaques and hyperphosphorylated tau tangles. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Triggering receptor expressed on myeloid cells-2 (TREM2) is an immune receptor expressed on microglia that also can become soluble (sTREM2). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The CSF and plasma cohorts were on average 71.4(±8.5) and 72.2 (±9.3) years of age, 49.1%/50.8% was female, and 263/453 (0.59%/51.8%) were cognitively impaired, respectively. 4 key findings →
Participants: 97 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neuronal dysfunction has been extensively studied as a central feature of neurodegenerative tauopathies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cellular cross-talk, mediated by membrane receptors and their ligands, is crucial for brain homeostasis and can contribute to neurodegenerative diseases such as Alzheimer’s disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD), the most common cause of dementia, is characterized by the accumulation of amyloid-β (Aβ) in senile plaques and abnormally hyperphosphorylated tau proteins in neurofibrillary tangles. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
However, it remains unknown whether white matter (WM) decline due to AD is associated with specific Tau phosphorylation site(s). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD)-modifying therapies are approved for treatment of early-symptomatic AD. 4 key findings →
Participants: 200 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Incorporating AD blood tests into screening for AD clinical trials may reduce the time and financial cost of enrollment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Accumulation of β-amyloid (Aβ) in the brain is a key event in Alzheimer disease pathogenesis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is characterized by neuronal loss and astrocytosis in the cerebral cortex. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Subtle changes in objective spatial navigation ability have been observed in the preclinical stage of Alzheimer disease (AD) cross-sectionally and have been found to predict clinical progression. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Finally, at the RHOJ locus, the rare allele was associated with increased tTau ( p ‐value=4.74×10 ‐05 ) and pTau181 ( p ‐value=4.07×10 ‐07 ), and decreased Aβ42/40 ratio ( p ‐value=4.32×10 ‐05 ). 2 key findings →
Participants: 91 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In this review we highlight recent advances in the human genetics of frontotemporal dementia (FTD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Primary and secondary tauopathies are major causes of dementia characterized by the abnormal accumulation of microtubule-associated protein tau. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Soluble triggering receptor expressed on myeloid cells 2 (sTREM2) levels in the cerebrospinal fluid (CSF) have been associated with Alzheimer disease (AD) status. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Increasing evidence suggests that accurate prediction of Alzheimer’s disease (AD) symptom onset requires more than amyloid- and tau-centric biomarkers such as cerebrospinal fluid (CSF) Aβ42/40, total tau and p-tau181 and plasma p-tau217. 4 key findings →
Participants: 484 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 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 →