27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
An unresolved question for the understanding of Alzheimer's disease (AD) pathophysiology is why a significant percentage of amyloid-β (Aβ)-positive cognitively unimpaired (CU) individuals do not develop detectable downstream tau pathology and, consequently, clinical deterioration. 5 key findings →
Design: cohort Participants: 1,016 Evidence: moderate
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Cancer survivors had a lower risk of Alzheimer's disease than those without cancer, and patients with Alzheimer's disease had a lower risk of incident cancer. 5 key findings →
Design: cohort study Participants: 1,278 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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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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Whether mild TBI (mTBI) in veterans confers a similar increased risk of AD is less known. 4 key findings →
Design: case-control study Participants: 51 Evidence: moderate
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HI is associated with increased risk of developing dementia in older adults. 3 key findings →
Evidence: high
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Physicians noted impairment in a minority of impaired patients. 3 key findings →
Design: cross-sectional Participants: 1,107 Evidence: low
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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
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This study of a large series of community-based incident dementia cases provides a way of judging the adequacy of currently available clinical diagnostic criteria. 2 key findings →
Participants: 134 Evidence: low
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These results provide evidence that, in the absence of significant neurodegenerative processes, individuals who harbor AD neuropathology may remain cognitively unimpaired. 4 key findings →
Design: cross-sectional Participants: 79 Evidence: low
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Clinico-pathological correlation studies and positron emission tomography amyloid imaging studies have shown that some individuals can tolerate substantial amounts of Alzheimer's pathology in their brains without experiencing dementia. 5 key findings →
Evidence: low
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None of the clinical criteria for VaD identified the same group of subjects. 2 key findings →
Participants: 52 Evidence: low
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Alzheimer's disease (AD), the most common form of dementia, remains challenging to understand and treat despite decades of research and clinical investigation. 3 key findings →
Evidence: low
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Cerebral amyloid angiopathy (CAA) is characterized by the deposition of the amyloid beta-protein (A beta) within cerebral vessels. 2 key findings →
Evidence: low
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18 F-SMBT-1 yielded high-contrast images at steady state (60-80 min after injection). 5 key findings →
Design: cross-sectional Evidence: low
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L-Arginine is the only endogenous nitrogen-containing substrate of NO synthase (NOS), and it thus governs the production of NO during nervous system development as well as in disease states such as stroke, multiple sclerosis, Parkinson's disease, and HIV dementia. 4 key findings →
Evidence: low
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Higher student-teacher ratio was associated with worse cognitive function and greater school year length was associated with better cognitive function. 5 key findings →
Participants: 433 Evidence: low
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Individuals with Down syndrome (DS) have an increased risk of developing Alzheimer disease (AD), with nearly all individuals exhibiting AD neuropathology, including amyloid beta (Aβ) plaques and neurofibrillary tangles (NFT), by age 40 years. 5 key findings →
Design: cross-sectional Participants: 98 Evidence: low
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Despite accumulating amyloid burden, cholinergic enzyme activity is stable in the precuneus during prodromal AD. 4 key findings →
Evidence: low
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Neuroplasticity involves molecular and structural changes in central nervous system (CNS) throughout life. 4 key findings →
Evidence: low
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Although the two pathological hallmarks of Alzheimer's disease (AD), senile plaques composed of amyloid-β (Aβ) peptides and neurofibrillary tangles (NFTs) consisting of hyperphosphorylated tau, have been studied extensively in postmortem AD and relevant animal and cellular models, the pathogenesis of AD remains unknown, particularly in the early stages of the disease where therapies presumably would be most effective. 2 key findings →
Evidence: low
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PurposeDelirium is a common yet preventable complication of hospitalization, surgery and illness that is associated with poor outcomes. 1 key finding →
Design: cohort study Evidence: moderate
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Mild cognitive impairment (MCI) is considered to be an early stage in the progression of Alzheimer's disease (AD) providing an opportunity to investigate brain pathogenesis prior to the onset of dementia. 5 key findings →
Evidence: low
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Over the past decade, public awareness of the long-term pathological consequences of traumatic brain injury (TBI) has increased. 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. 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 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 →