28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Genetic variants in the triggering receptor expressed on myeloid cells 2 (TREM2) have been linked to Nasu-Hakola disease, Alzheimer's disease (AD), Parkinson's disease, amyotrophic lateral sclerosis, frontotemporal dementia (FTD), and FTD-like syndrome without bone involvement. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
This study reviewed the structure, function, analytical aspects, and age-dependent normal ranges of neurofilaments, providing a comprehensive overview of neurofilament light chain as a marker of axonal injury across various neurological disorders. 2 key findings →
Full summary, score breakdown and related studies → Original source Free full text
Copy-number variants (CNVs) are major contributors to human disease. 2 key findings →
Design: case-control Participants: 22,319 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our data suggest that [F-18]-AV-1451 holds promise as a surrogate marker for the detection of brain tau pathology in the form of tangles and paired helical filament-tau-containing neurites in Alzheimer brains but also point to its relatively lower affinity for lesions primarily made of straight tau filaments in non-Alzheimer tauopathy cases and to the existence of some [F-18]-AV-1451 off-target binding. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our findings suggest that inflammation in the CNS increases in normal aging and is intimately related to markers of neurodegeneration in the preclinical stages of AD and SNAP. sAPPβ and β-secretase activity are not useful diagnostic or staging markers in preclinical AD. 2 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Individuals with neuropsychiatric, cardiovascular, and sensory impairment/cancer patterns are at increased risk for dementia and APOE ε4, and inflammation may further increase the risk. 3 key findings →
Participants: 2,478 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our data suggest that interactions between biomarkers in AD result in a 2-phase phenomenon of pathological cortical thickening associated with low CSF Aβ, followed by atrophy once CSF p-tau becomes abnormal. 3 key findings →
Design: cross-sectional Participants: 145 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
MRI studies have provided valuable insights into the structure and function of neural networks, particularly in health and in classical neurodegenerative conditions such as Alzheimer disease. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The concept of diabetic retinopathy as a microvascular disease has evolved, in that it is now considered a more complex diabetic complication in which neurodegeneration plays a significant role. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Plasma p-tau212 might have utility for theragnostics, monitoring therapy efficacy, and as a target engagement biomarker in clinical trials both in sporadic and DSAD. 1 key finding →
Participants: 245 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Symptomatic females with genetic FTD had lower frontal cortical thickness than males, and the C9orf72 subgroup showed lower-than-expected frontal cortical thickness for a given level of executive functioning. 5 key findings →
Design: longitudinal study Participants: 394 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Blood-based biomarkers offer a major advance in the clinical evaluation of neurodegenerative diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We found increased levels of YKL-40 and decreased levels of sAPPβ in both FTD and ALS groups compared to controls. 2 key findings →
Design: cross-sectional Participants: 86 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Individuals with DS were more likely to have microbleeds than controls (20% vs 8.9%, p 60 years) and AD clinical stage (12.42% asymptomatic, 27.9% prodromal, 35.09% dementia) were more common in APOE ε4 carriers (26% vs 18.3% noncarriers, p = 0.008), but not associated with vascular risk factors ( p > 0.05). 4 key findings →
Design: cross-sectional Participants: 276 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The NutriAlz program had no effect on functional decline in Alzheimer disease patients living at home over one year, but reduced the risk for malnutrition, as recommendations concerning diet and exercise were provided. 2 key findings →
Participants: 448 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Almost all individuals with Down Syndrome (DS) develop Alzheimer's disease (AD) by mid to late life. 3 key findings →
Participants: 229 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Autosomal-dominant Alzheimer disease (ADAD) is a genetic disorder caused by mutations in Amyloid Precursor Protein (APP) or Presenilin (PSEN) genes. 4 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The shared role of amyloid-β (Aβ) deposition in cerebral amyloid angiopathy (CAA) and Alzheimer disease (AD) is arguably the clearest instance of crosstalk between neurodegenerative and cerebrovascular processes. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Forty-three proteins were differentially regulated in FTD compared to controls and AD, reflecting axon development, regulation of synapse assembly, and cell-cell adhesion mediator activity pathways. 5 key findings →
Participants: 189 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Low baseline Aβ42/Aβ40 was significantly associated with increased amyloid accumulation (β = 0.257, 95% confidence interval (CI) 0.177-0.336, P < 0.001), and with higher risk of conversion to Aβ-PET positivity (Hazard ratio (HR) = 2.84, 95% CI 1.14-7.04, P = 0.025) and to MCI due to AD (HR = 3.25, 95% CI 1.17-9.01, P = 0.024). 5 key findings →
Design: longitudinal study Participants: 200 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Individuals with Down syndrome (DS) have a genetically determined form of Alzheimer's disease (AD) due to the amyloid precursor protein (APP) gene dose effect. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) reduces associative effects on false recognition in the Deese-Roediger-McDermott task, either due to impaired memory for gist or impaired use of gist in memory decisions. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Soluble triggering receptor expressed on myeloid cells 2 (sTREM2) in cerebrospinal fluid (CSF) has been associated with Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our proof-of-concept study is the first to show that microstructural and macrostructural changes can reflect underlying neuroinflammatory mechanisms in early stages of Alzheimer disease (AD). 2 key findings →
Participants: 31 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These findings highlight LBP prevalence in DSAD but suggest current SAA may fail to detect limited αSyn deposition. 4 key findings →
Participants: 270 Evidence: moderate
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 →