Participants were 60 (range 44-74) years old with 38 (30-51) years' T1D duration. 3 key findings →
Participants: 373 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Participants were 60 (range 44-74) years old with 38 (30-51) years' T1D duration. 3 key findings →
Participants: 373 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Several potential disease-modifying drugs for Alzheimer's disease (AD) have failed to show any effect on disease progression in clinical trials, conceivably because the AD subjects are already too advanced to derive clinical benefit from treatment and because diagnosis based on clinical criteria alone introduces a high misdiagnosis rate. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our goal was to ascertain the involvement of the temporal lobe in the preclinical (not yet diagnosable) stages of dementia of the Alzheimer's type (DAT) by using MRI-derived volumes. 2 key findings →
Design: cross-sectional Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neurogenic orthostatic hypotension (nOH) is common in patients with neurodegenerative disorders such as Parkinson's disease, multiple system atrophy, pure autonomic failure, dementia with Lewy bodies, and peripheral neuropathies including amyloid or diabetic neuropathy. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neuropsychiatric symptoms (NPSs) are hallmarks of Alzheimer's disease (AD), causing substantial distress for both people with dementia and their caregivers, and contributing to early institutionalization. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The Electrophysiology Professional Interest Area (EPIA) and Global Brain Consortium endorsed recommendations on candidate electroencephalography (EEG) measures for Alzheimer's disease (AD) clinical trials. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Early diagnosis of Alzheimer's disease plays a pivotal role in patient care and clinical trials. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Research increasingly suggests that subjective cognitive decline (SCD) in older adults, in the absence of objective cognitive dysfunction or depression, may be a harbinger of non-normative cognitive decline and eventual progression to dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These results are approximately 10 times those usually observed with both nonpharmacological and pharmacological treatments and indicate substantial benefits with the management program for advanced AD persons. 3 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
None of the participants were diabetics, smokers, or met criteria for obesity. 4 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Defective autophagy contributes to Alzheimer disease (AD) pathogenesis although evidence is conflicting on whether multiple stages are impaired. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Nuclear clearance and cytoplasmic aggregation of TAR DNA-binding protein 43 (TDP-43) are observed in many neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Patients with trisomy 21 [Down syndrome (DS)] progressively develop amyloid beta-protein (A beta) deposits and then other features of Alzheimer's disease (AD), apparently due to increased gene dosage and thus expression of the beta-amyloid precursor protein.
Full summary, score breakdown and related studies → Original source Free full text
Extracellular deposition of the beta/A4 amyloid peptide is a characteristic feature of the brain in patients with Alzheimer disease. beta/A4 amyloid is derived from the amyloid precursor protein (APP), an integral membrane protein that exists as three major isoforms (APP695, APP751, and APP770). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Familial Danish dementia (FDD), also known as heredopathia ophthalmo-oto-encephalica, is an autosomal dominant disorder characterized by cataracts, deafness, progressive ataxia, and dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A major feature of Alzheimer's disease (AD) is the loss of noradrenergic locus coeruleus (LC) projection neurons that mediate attention, memory, and arousal. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Study objectives Emerging evidence suggests a role for sleep in contributing to the progression of Alzheimer disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The QDRS provides a rapid method to determine study eligibility; stage patients in clinical practice; and improve case ascertainment in population studies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These data support the hypothesis that neuronal endosomal dysfunction is associated with preclinical AD. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Older age was associated with greater odds of abnormal p-Tau217 (odds ratio [OR] 1.08 per year, 95% CI 1.07–1.09), as was APOE ε4 carrier status (OR 3.32, 95% CI 2.65–4.17). 5 key findings →
Design: cross-sectional Participants: 2,798 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Study objectives To evaluate the role of orexin-A with respect to cerebrospinal fluid (CSF) Alzheimer disease (AD) biomarkers, and explore its relationship to cognition and sleep characteristics in a group of cognitively normal elderly individuals. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neuroplasticity involves molecular and structural changes in central nervous system (CNS) throughout life. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Although the two pathological hallmarks of Alzheimer's disease (AD), senile plaques composed of amyloid-β (Aβ) peptides and neurofibrillary tangles (NFTs) consisting of hyperphosphorylated tau, have been studied extensively in postmortem AD and relevant animal and cellular models, the pathogenesis of AD remains unknown, particularly in the early stages of the disease where therapies presumably would be most effective. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The metabolic fate of the Alzheimer beta/A4 amyloid precursor protein (APP) includes intraamyloid proteolysis that leads to the production of secreted N-terminal and cell-associated C-terminal fragments. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These findings lay groundwork to enable AD clinical trials with characterization and disease-specific tracking of DS adults. 3 key findings →
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.
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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.
1,048 records (3.3% of the library) are not peer-reviewed — 973 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events