Atrophy rates are pathologically increased up to seven years before "expected onset". 1 key finding →
Participants: 94 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Atrophy rates are pathologically increased up to seven years before "expected onset". 1 key finding →
Participants: 94 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
By 2050, the American 85 years old and over population will triple. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This pilot trial justifies KD studies in mild Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Goal 1 of the National Plan to Address Alzheimer's Disease is to prevent and effectively treat Alzheimer disease and Alzheimer disease-related dementias by 2025. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Higher arterial stiffness and pulsatility were associated with MCI and dementia in white participants. 3 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Reduced f0 range reflects impaired prosody in bvFTD. 3 key findings →
Participants: 32 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The conventional Clock Drawing Test (cCDT) is a rapid and inexpensive screening tool for detection of moderate and severe dementia. 4 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The increase in the prevalence of obesity represents a worldwide phenomenon in all age groups and is pathologically and genetically correlated with several metabolic and cardiovascular diseases, representing the most frequent age-related diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
People with Down syndrome (DS) are at high risk for developing Alzheimer disease (AD) with age. 2 key findings →
Participants: 32 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Over the past decade, a surge of evidence has documented various pathological processes in the retina of patients suffering from mild cognitive impairment, Alzheimer's disease (AD), Parkinson's disease (PD), and other neurodegenerative diseases. 1 key finding →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Conventional genetic approaches and computational strategies have converged on immune-inflammatory pathways as key events in the pathogenesis of late onset sporadic Alzheimer's disease (LOAD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Higher gLFC connectivity is a functional substrate of CR that helps to maintain episodic memory relatively well in the face of emerging FDG-PET hypometabolism in early-stage AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Molecular subtypes of sporadic CJD show different levels of plasma tau. 2 key findings →
Participants: 132 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Accumulating evidence suggests that genetic variants in the SORL1 gene are associated with Alzheimer disease (AD), but a strategy to identify which variants are pathogenic is lacking. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Affective symptoms are of prognostic utility, but interventions to prevent dementia syndromes are limited. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Though results of pivotal studies in early (prodromal/mild) Alzheimer's disease are awaited, results to date in more established (mild to moderate) Alzheimer's disease have been equivocal and no disease modifying agents are either licensed or can be currently recommended for clinical use. 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The most definitive classification systems for dementia are based on the underlying pathology which, in turn, is categorized largely according to the observed accumulation of abnormal protein aggregates in neurons and glia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In contrast to the idea that hippocampal and amygdala volume loss occur in late phases of neurodegeneration, recent contributions point to the relevance of preexisting structural deficits that are associated with aging and are independent of amyloid deposition in preclinical Alzheimer disease cases. 5 key findings →
Participants: 455 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
CMBs are a common vascular pathology in the elderly. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyloid-beta (Aβ) plays a key role in the pathogenesis of Alzheimer's disease (AD), but little is known about the proteoforms present in AD brain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dementia prevalence estimates were higher than expected for this low-income rural community. 3 key findings →
Participants: 1,051 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our data suggest that some degree of blood-brain barrier dysfunction is common in older people and that this may be related to clinical dementia risk, additional to standard MRI biomarkers. 5 key findings →
Participants: 126 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Metabolic dysfunction is a well-established feature of Alzheimer's disease (AD), evidenced by brain glucose hypometabolism that can be observed potentially decades prior to the development of AD symptoms. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Approximately 70 human RNA-binding proteins (RBPs) contain a prion-like domain (PrLD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
See Grinberg and Heinsen (doi:10.1093/brain/awx261) for a scientific commentary on this article. 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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →