27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Participants had a mean age of 73.4 years; 62.7% were women, and 34.9% were Hispanic or nonwhite. 5 key findings →
Design: randomized controlled trial Participants: 126 Evidence: high
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Plasma tau partly reflects AD pathology, but the overlap between normal aging and AD is large, especially in patients without dementia. 3 key findings →
Design: longitudinal study Participants: 179 Evidence: moderate
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During a mean (SD) follow-up of 6.1 (3.2) years, 1601 participants had no hospitalization, 1287 had 1 or more noncritical illness hospitalizations, and 41 had 1 or more critical illness hospitalizations. 4 key findings →
Design: cohort study Participants: 2,929 Evidence: moderate
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Cox proportional hazards regression, adjusted for age at baseline, gender, apolipoprotein genotype, and NYU paragraph delayed recall score, showed that higher BDI scores were associated with progression to AD (p = 0.03). 4 key findings →
Participants: 208 Evidence: low
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The frequent association of chronic traumatic encephalopathy with other neurodegenerative disorders suggests that repetitive brain trauma and hyperphosphorylated tau protein deposition promote the accumulation of other abnormally aggregated proteins including TAR DNA-binding protein 43, amyloid beta protein and alpha-synuclein. 1 key finding →
Participants: 85 Evidence: moderate
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In this longitudinal study of cognitively unimpaired adults, living in the most highly disadvantaged neighborhoods was associated with accelerated degeneration in Alzheimer signature regions and cognitive decline. 5 key findings →
Design: longitudinal study Participants: 19 Evidence: moderate
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Although the presence of abnormal levels of amyloid-β (Aβ) is associated with higher rates of progression to clinically classified mild cognitive impairment or dementia, little research has evaluated potentially modifiable moderators of Aβ-related cognitive decline, such as anxiety and depressive symptoms. 5 key findings →
Design: cohort study Participants: 333 Evidence: moderate
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The relationship between sensory impairment and cognitive impairment was not unique to one sensory system, suggesting that sensorineural health may be a marker of brain aging. 2 key findings →
Design: longitudinal study Participants: 1,884 Evidence: moderate
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The sample consisted of 447 decedents (249 men [56%]; mean [SD] age, 80.3 [9.5] years; median year of death, 2011) spanning 24 years of donation. 5 key findings →
Design: cross-sectional Participants: 24 Evidence: low
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Cardiovascular risk factors often cluster into a metabolic syndrome that may increase the risk of dementia. 2 key findings →
Design: cohort study Evidence: moderate
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A slower rate of hippocampal atrophy in normal APOE2 carriers is consistent with the lower risk of Alzheimer disease in these individuals. 5 key findings →
Design: cohort study Participants: 72 Evidence: moderate
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Inclusion and exclusion criteria were met in 303 patients, and 25 (8.3%) presented to the ED with delirium. 1 key finding →
Design: cross-sectional Participants: 303 Evidence: low
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Chronic traumatic encephalopathy (CTE) is a neurodegeneration characterized by the abnormal accumulation of hyperphosphorylated tau protein within the brain. 2 key findings →
Evidence: low
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In addition to known candidate genes, APOE, TOMM40, and one hypothetical gene LOC100129500 partially overlapping APOE; one novel gene, EPC2, and several other interesting genes were associated with CSF biomarkers that are related to AD. 3 key findings →
Participants: 374 Evidence: moderate
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In AD patients with symptoms of psychosis, agitation, or aggressive behavior, medications can have a small but significant impact on caregiver burden. 4 key findings →
Design: clinical trial Participants: 361 Evidence: high
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In this retrospective study, GAP-43 was measured in participants from the AD Neuroimaging Initiative (ADNI) cohort using an in-house ELISA method, and levels were compared between groups, both cross-sectionally and longitudinally. 4 key findings →
Participants: 786 Evidence: moderate
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Alzheimer's disease is the most common cause of dementia worldwide, with the prevalence continuing to grow in part because of the aging world population. 1 key finding →
Evidence: low
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Frontotemporal dementia and Alzheimer disease display different spatial distributions of hypoperfusion on arterial spin labeling MRI. 2 key findings →
Design: cross-sectional Participants: 21 Evidence: low
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This preliminary report describes the development, reliability, and validity testing of the Geriatric Depression Scale (GDS) designed specifically for rating depression in the elderly. 3 key findings →
Evidence: low
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Twenty patients with AD and 25 CN subjects had MRI scans and clinical evaluations twice approximately 1.9 years apart. 1 key finding →
Evidence: low
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Diagnosis frequency ranged across HRRs from 0.58 chronic conditions in Grand Junction, Colorado, to 1.23 in Miami, Florida (mean, 0.90 [95% confidence interval {CI}, 0.89-0.91]; median, 0.87 [interquartile range, 0.80-0.96]). 5 key findings →
Design: cross-sectional Evidence: low
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In vivo biomarkers for detecting neuropathologies from repetitive head impacts (RHI), including chronic traumatic encephalopathy (CTE), are needed. 4 key findings →
Design: case-control study Participants: 231 Evidence: moderate
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This comprehensive population genetic study in control subjects fills the void for a PARK2 reference dataset. 3 key findings →
Participants: 1,686 Evidence: low
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Revised diagnostic criteria for Alzheimer disease (AD) acknowledge a key role of imaging biomarkers for early diagnosis. 5 key findings →
Evidence: low
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The presence of tangles of abnormally phosphorylated tau is a characteristic of Alzheimer's disease (AD), and the loss of synapses correlates with the degree of dementia. 4 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 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 →