Increasing evidence suggests a role of atherosclerosis in the pathogenesis of cognitive impairment and dementia. 4 key findings →
Participants: 844 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Increasing evidence suggests a role of atherosclerosis in the pathogenesis of cognitive impairment and dementia. 4 key findings →
Participants: 844 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In the general population, we investigated the association of a recently developed cerebral small vessel disease (CSVD) sum score with stroke, dementia, and mortality. 4 key findings →
Participants: 66 Evidence: low
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The Framingham Heart Study has enrolled 3 generations of participants, the original cohort (gen 1) enrolled in 1948, the offspring cohort (gen 2) enrolled in 1971 and the third generation enrolled in 2002. 4 key findings →
Participants: 59 Evidence: moderate
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A family history of Alzheimer's disease (AD) increases one's risk of developing late-onset AD (LOAD), and a maternal family history of LOAD influences risk more than a paternal family history. 4 key findings →
Design: cross-sectional Participants: 99 Evidence: low
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Neuropsychiatric symptoms, also known as behavioral and psychological symptoms of dementia (BPSD), affect the majority of patients with dementia, and result in a greater cognitive and functional impairment. 4 key findings →
Participants: 657 Evidence: moderate
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Recent interest in enlarged perivascular spaces (ePVS) in the brain, which can be visualized on MRI and appear isointense to cerebrospinal fluid on all sequence weightings, has resulted in the necessity of reliable algorithms for automated segmentation to allow for whole brain assessment of ePVS burden. 4 key findings →
Participants: 14 Evidence: moderate
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Late-life depression (LLD) is associated with development of different types of dementia. 4 key findings →
Participants: 185 Evidence: low
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Age and female sex are risk factors for dementia, and menopause is associated with cognitive dysfunction. 4 key findings →
Design: cross-sectional Evidence: low
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The duration and lifetime pattern of hypertension is related to risk of stroke and dementia. 4 key findings →
Participants: 1,686 Evidence: moderate
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Alzheimer's Disease (AD), one of the main causes of death in elderly people, is characterized by Mild Cognitive Impairment (MCI) at prodromal stage. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is characterised by a dynamic process of neurocognitive changes from normal cognition to mild cognitive impairment (MCI) and progression to dementia. 4 key findings →
Evidence: moderate
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Multimorbidity (the presence of two or more long-term conditions [LTCs]) was suggested to exacerbate the neuronal injuries. 4 key findings →
Evidence: low
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A decline in instrumental activities of daily living (IADL) correlates with the progression from mild cognitive impairment (MCI) to Alzheimer's disease (AD) dementia and has been associated with frontal and parietal hypometabolism, lower cerebrospinal fluid amyloid β 1-42 , and inferior temporal cortical thinning. 4 key findings →
Design: cross-sectional Evidence: low
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The differential diagnosis of frontotemporal dementia (FTD) and Alzheimer's disease (AD) is difficult due to the overlaps of clinical symptoms. 4 key findings →
Participants: 47 Evidence: low
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The subject groups for model derivation comprised 80 healthy subjects (HS), 36 patients with mild cognitive impairment (MCI) who converted to AD dementia within 18 months, 85 non-converter MCI patients who did not convert within 24 months, and 67 AD dementia patients with baseline FDG PET scan were recruited from the AD Neuroimaging Initiative (ADNI) database. 4 key findings →
Participants: 36 Evidence: moderate
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Alzheimer's disease acknowledged as progressive multifarious neurodegenerative disorder, is the leading cause of dementia in late adult life. 4 key findings →
Evidence: low
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There are dozens of drugs in development for AD with billions of dollars invested. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is a devastating dementia of late life that is correlated with a region-specific neuronal cell loss. 4 key findings →
Evidence: low
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Chronic Traumatic Encephalopathy (CTE) is a neurodegenerative disease thought to be caused, at least in part, by repetitive brain trauma, including concussive and subconcussive injuries. 4 key findings →
Evidence: low
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Frontotemporal dementia with inclusion body myopathy and Paget disease of bone is a rare, autosomal-dominant disorder caused by mutations in the gene valosin-containing protein (VCP). 4 key findings →
Evidence: low
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Traumatic brain injury (TBI) increases susceptibility to Alzheimer's disease (AD), but it is not known how TBI contributes to the onset or progression of this common late life dementia. 4 key findings →
Participants: 15 Evidence: low
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Early-onset Alzheimer disease (EOAD), with onset in individuals younger than 65 years, although overshadowed by the more common late-onset AD (LOAD), differs significantly from LOAD. 3 key findings →
Evidence: low
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Mutations in RNA-binding proteins (RBPs) localized in ribonucleoprotein (RNP) granules, such as hnRNP A1 and TDP-43, promote aberrant protein aggregation, which is a pathological hallmark of various neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 4 key findings →
Evidence: low
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TAR DNA binding protein-43 (TDP-43) is found in ubiquitinated inclusions (UBIs) in some frontotemporal dementias (FTD-U). 4 key findings →
Evidence: low
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Accumulation and aggregation of amyloid-β (Aβ) peptides in the brain trigger the development of progressive neurodegeneration and dementia associated with Alzheimer's disease (AD). 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →