There is no evidence for individual risk prediction and even less for specific treatments. 5 key findings →
Evidence: moderate
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27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
There is no evidence for individual risk prediction and even less for specific treatments. 5 key findings →
Evidence: moderate
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In the absence of disease modifying therapies for dementia, the question rises what the benefits are of an early dementia diagnosis for patients and their caregivers. 1 key finding →
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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Accumulation of tau is a critical event in several neurodegenerative disorders, collectively known as tauopathies, which include Alzheimer's disease and frontotemporal dementia. 2 key findings →
Evidence: low
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Metabolic disorders and aging promote accumulation of amylin amyloid in the cerebrovascular system and gray matter, altering microvasculature and tissue structure. 2 key findings →
Evidence: low
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Alzheimer's disease (AD) is the leading cause of dementia and has no cure. 4 key findings →
Evidence: low
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Alzheimer disease (AD) is an age-related neurodegenerative disease. 4 key findings →
Evidence: low
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Triggering receptor expressed on myeloid cells-2 (TREM2) and its signaling adaptor protein TYROBP/DAP12 play important roles in signal transduction in dendritic cells, osteoclasts, tissue macrophages, and microglia. 4 key findings →
Evidence: low
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Late-onset Alzheimer's disease (AD) is a sporadic disorder with increasing prevalence in aging. 4 key findings →
Evidence: low
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Exposure to vascular risk factors has a gradual deleterious effect on brain MRI and cognitive measures. 4 key findings →
Participants: 55 Evidence: moderate
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The interstitial fluid (ISF) drainage pathway has been hypothesized to underlie the clearance of solutes and metabolites from the brain. 4 key findings →
Evidence: low
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Aggregates of hyperphosphorylated tau (PHF-tau), such as neurofibrillary tangles, are linked to the degree of cognitive impairment in Alzheimer's disease.
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Aggregates of hyperphosphorylated tau (PHF-tau), such as neurofibrillary tangles, are linked to the degree of cognitive impairment in Alzheimer's disease.
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In vivo quantification of β-amyloid deposition using positron emission tomography is emerging as an important procedure for the early diagnosis of the Alzheimer's disease and is likely to play an important role in upcoming clinical trials of disease modifying agents.
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Dysphagia is a major health care problem in nursing homes. 2 key findings →
Participants: 395 Evidence: low
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Hypothalamic-pituitary-adrenal axis hyperresponsiveness and a less frequent suppression of the GH/IGF-1 axis in response to acute stress are possibly involved in delirium pathophysiology. 2 key findings →
Participants: 101 Evidence: low
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Awareness of the terminal nature of dementia may improve patient comfort at the end of life. 2 key findings →
Participants: 372 Evidence: low
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Exposure to maternal anxiety predicts offspring brain development. 1 key finding →
Participants: 175 Evidence: low
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Enlarged perivascular spaces are associated with age, lacunar stroke subtype and white matter lesions and should be considered as another magnetic resonance imaging marker of cerebral small vessel disease. 3 key findings →
Participants: 298 Evidence: low
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Parkinson's disease (PD), following Alzheimer's disease, is the second-most common neurodegenerative disorder in the United States. 5 key findings →
Participants: 630,000 Evidence: low
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Given the importance of identifying dementia prodromes for future treatment efforts, we examined two methods of diagnosing mild cognitive impairment (MCI) and determined whether empirically-derived MCI subtypes of these diagnostic methods were consistent with one another as well as with conventional MCI subtypes (i.e., amnestic, non-amnestic, single-domain, multi-domain). 2 key findings →
Participants: 134 Evidence: low
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Amyloid PET imaging is a novel diagnostic test that can detect in living humans one of the two defining pathologic lesions of Alzheimer disease, amyloid-β deposition in the brain. 3 key findings →
Evidence: low
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Human apolipoprotein E (apoE) has 3 isoforms: apoE2, apoE3, and apoE4. 1 key finding →
Evidence: low
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In an aging population with increasing incidence of dementia and cognitive impairment, strategies are needed to slow age-related decline and reduce disease-related cognitive impairment in older adults. 1 key finding →
Evidence: low
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Our results revealed disease severity-related alterations of the thalamo-default mode network and thalamocortical connectivity in AD and MCI patients. 4 key findings →
Participants: 35 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. 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 →