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
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
[(11)C]PIB retention in the neocortical and subcortical brain regions was significantly higher in AD patients than in age-matched controls. 3 key findings →
Participants: 97 Evidence: low
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Measures of neuronal damage/dysfunction are likely good surrogates for disease progression in Alzheimer disease (AD). 4 key findings →
Participants: 60 Evidence: low
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Physical performance tests are important for assessing the effect of physical activity interventions in older people with dementia, but their psychometric properties have not been systematically established within this specific population. 4 key findings →
Design: cross-sectional Participants: 58 Evidence: low
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Hippocampal volumetry derived from structural MRI is increasingly used to delineate regions of interest for functional measurements, assess efficacy in therapeutic trials of Alzheimer's disease (AD) and has been endorsed by the new AD diagnostic guidelines as a radiological marker of disease progression. 4 key findings →
Design: longitudinal study Evidence: moderate
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The acute and long-term consequences of traumatic brain injury (TBI) have received increased attention in recent years. 3 key findings →
Evidence: low
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Late onset Alzheimer's disease (LOAD) etiology is influenced by complex interactions between genetic and environmental risk factors. 4 key findings →
Evidence: low
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We have used a translational convergent functional genomics (CFG) approach to identify and prioritize genes involved in schizophrenia, by gene-level integration of genome-wide association study data with other genetic and gene expression studies in humans and animal models. 3 key findings →
Evidence: low
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The C9orf72 expansion is a common cause of ALS and FTLD, but not of AD or PD. 4 key findings →
Participants: 520 Evidence: low
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Dementia, a major cause of disability and institutionalization in older people, poses a serious threat to public health and to the social and economic development of modern society. 2 key findings →
Evidence: high
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Increased (11)C-DED binding throughout the brain of the MCI (11)C-PIB+ patients potentially suggests that astrocytosis is an early phenomenon in AD development. 2 key findings →
Evidence: low
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Stepwise decreases in WM integrity as measured by both DTI and FLAIR were independently associated with stepwise increases in WMH risk, emphasizing that these modalities may provide complementary information for understanding the time course of aging-associated WM degeneration. 3 key findings →
Design: longitudinal study Evidence: moderate
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The long-chain ω-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are potential candidates for interventions to delay Alzheimer disease (AD), but evidence from clinical studies is mixed. 1 key finding →
Participants: 281 Evidence: low
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The Minority Aging Research Study (MARS) is a longitudinal, epidemiologic cohort study of decline in cognitive function and risk of Alzheimer's disease (AD) in older African Americans, with brain donation after death added as an optional component for those willing to consider organ donation. 1 key finding →
Design: cohort study Evidence: moderate
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AMI is the first French longitudinal study on health and aging set up in a population of elderly farmers living in rural area through a multidisciplinary approach. 5 key findings →
Design: longitudinal study Evidence: moderate
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A motor-based MCR syndrome provides a clinical approach to identify individuals at high risk for dementia, especially vascular dementia, to target for further investigations and who may benefit from preventive interventions. 3 key findings →
Evidence: low
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Behavioral and psychological symptoms of dementia (BPSD), also known as neuropsychiatric symptoms, represent a heterogeneous group of non-cognitive symptoms and behaviors occurring in subjects with dementia. 3 key findings →
Evidence: low
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Prions are self-templating protein conformers that are naturally transmitted between individuals and promote phenotypic change. 5 key findings →
Evidence: low
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The accumulation of Tau into aggregates is associated with key pathological events in frontotemporal lobe degeneration (FTD-Tau) and Alzheimer disease (AD). 3 key findings →
Evidence: low
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Fornix FA both cross-sectionally correlated with and longitudinally predicted memory decline and progression to AD. 1 key finding →
Design: cross-sectional Evidence: low
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[(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
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Accumulations of insoluble deposits of amyloid β-peptide are major pathological hallmarks of Alzheimer disease. 4 key findings →
Evidence: low
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Although amyloid-beta (Aβ) peptide deposition into insoluble plaques is a pathological hallmark of Alzheimer disease; soluble oligomeric Aβ has been hypothesized to more directly underlie impaired learning and memory in dementia of the Alzheimer type. 4 key findings →
Evidence: low
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Disability is commonly considered as an irreversible condition of advanced age. 4 key findings →
Participants: 65 Evidence: low
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PiB and florbetapir retention ratios were strongly associated in the same individuals, and this relationship was consistent across several data analysis methods, despite scan-rescan intervals of more than a year.
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →