27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Investigation of dopaminergic transporter loss in vivo using (123)I-N-fluoropropyl-2β-carbomethoxy-3β-(4-iodophenyl) nortropane single photon emission computed tomography has been widely used as a diagnostic aid in Lewy body disease. 3 key findings →
Evidence: moderate
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In this group of older adults free from neurodegenerative diseases, a greater variability of step length was associated with greater burden of subclinical brain vascular abnormalities as defined by MRI. 3 key findings →
Evidence: moderate
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The majority of patients with Parkinson's Disease develop Dementia (PDD) in late stages of the disease and have widespread neocortical distribution of alpha-synuclein pathology at autopsy, compared with PD without dementia, in which neocortical synuclein pathology is less prevalent. 4 key findings →
Evidence: low
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Wishes and preferences of people with dementia and their family carers may differ. 2 key findings →
Evidence: low
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The results suggest that education is robustly associated with level of cognitive function but not with rate of cognitive decline and that the former association primarily accounts for education's correlation with risk of dementia in old age. 2 key findings →
Evidence: low
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Algorithmic diagnoses provide a cost-effective way to conduct dementia research. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is the most frequent cause of dementia, where the abnormal accumulation of beta-amyloid (Aβ) and tau lead to neurodegeneration as well as loss of cognitive, behavioral, and functional abilities. 5 key findings →
Evidence: low
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We describe the history, development, and success of the recruitment and screening procedures used by researchers at the University of California, Davis Alzheimer's Disease Center (UCD ADC) to facilitate minority enrollment in research. 5 key findings →
Design: longitudinal study Evidence: moderate
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When compared to edentulous elderly patients, patients with remaining teeth were younger at admittance, were more often non-cooperative, and had a poorer oral health and higher need for dental care. 5 key findings →
Participants: 725 Evidence: low
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Alzheimer disease (AD) is the most common cause of dementia in people over 60 years old. 5 key findings →
Evidence: low
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The incidence of obesity in middle age is increasing markedly, and in parallel the prevalence of metabolic disorders including cardiovascular disease and type II diabetes is also rising. 1 key finding →
Evidence: low
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These Canadian estimates of the prevalence of dementia fall toward the upper end of the ranges in other studies, whereas the estimates for Alzheimer's disease fall in the middle of the ranges. 2 key findings →
Participants: 9,008 Evidence: low
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These observations provide cellular evidence to support the hypothesis that dendritic spine plasticity is a mechanism of cognitive resilience that protects older individuals with AD pathology from developing dementia. 4 key findings →
Evidence: low
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This study provides pathological validation that the new criteria assist with separating PPA cases with AD pathology into the new lv-PPA syndrome and found that a number of diagnostic clinical features (disinhibition, food preferences and naming) did not assist in discriminating the different FTD syndromes. 2 key findings →
Evidence: low
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Parkinson's disease dementia is neuropathologically characterized by aggregates of α-synuclein (Lewy bodies) in limbic and neocortical areas of the brain with additional involvement of Alzheimer's disease-type pathology. 4 key findings →
Evidence: low
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Predictive models may help differentiate MSA and PD premortem. 1 key finding →
Evidence: low
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This review should serve as a compendium of updated information on VaD and provide guidance in terms of newer diagnostic and potential therapeutic approaches. 2 key findings →
Design: narrative review Evidence: low
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Comprehension of insincere communication is an important aspect of social cognition requiring visual perspective taking, emotion reading, and understanding others' thoughts, opinions, and intentions. 2 key findings →
Participants: 102 Evidence: low
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Clinical trials focusing on therapeutic candidates that modify β-amyloid (Aβ) have repeatedly failed to treat Alzheimer's disease (AD), suggesting that Aβ may not be the optimal target for treating AD. 2 key findings →
Evidence: low
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During life, patients with AD pathology may be misdiagnosed with bvFTD if they have an early age at onset and prominent neuropsychiatric features despite having greater memory difficulties and more intact personality and executive functions than patients with bvFTD-FTLD. 2 key findings →
Participants: 23 Evidence: low
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Changes in delta bandpower showed the highest and most consistent pattern of correlations with longitudinal changes in neuropsychological testing. 2 key findings →
Design: longitudinal study Evidence: moderate
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Young onset Alzheimer's disease (YOAD) is defined as symptom onset before the age of 65 years and is particularly associated with phenotypic heterogeneity. 3 key findings →
Participants: 26 Evidence: low
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Ageing societies and a rising prevalence of dementia are associated with increasing demand for care home places. 2 key findings →
Evidence: low
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New personalized endpoints that are clinically meaningful to individuals and their families should be developed. 1 key finding →
Evidence: low
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Progressive supranuclear palsy (PSP) and cortocobasal degeneration (CBD) are often clinically confused with each other because they share a rapid disease progression, parkinsonism that responds poorly or transiently to levodopa therapy, and associated signs (e.g., ocular abnormalities, pyramidal signs and cognitive involvement). 5 key findings →
Participants: 51 Evidence: low
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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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →