In 1906, Alois Alzheimer first described the neuropathological hallmarks of the disease that now bears his name. 2 key findings →
Participants: 62 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
In 1906, Alois Alzheimer first described the neuropathological hallmarks of the disease that now bears his name. 2 key findings →
Participants: 62 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Neurodegenerative dementias with behavioral clinical presentation are a diverse group of diseases. 4 key findings →
Participants: 20 Evidence: moderate
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Stroke and dementia are leading causes of death and disability worldwide, requiring enhanced preventive strategies. 1 key finding →
Evidence: low
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Early and accurate diagnosis of dementia is essential to improving patient outcomes and reducing societal burden. 1 key finding →
Participants: 164 Evidence: low
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For MCI, MoCA cut-offs were 24 (three methods) and 25 (Youden's J Index). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our studies showed that DC and DRs in VD and AD groups were significantly lower than those in controls, while AC values were significantly higher. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The observation group had significantly lower Self-Rating Anxiety Scale (SAS) and Self-Rating Depression Scale (SDS) scores than the control group (both P<0.001). 5 key findings →
Participants: 45 Evidence: low
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DNA methylation, mRNA and protein levels, and cognitive performance using the Mini-Mental State Examination (MMSE) and Clock Drawing Test (CDT). 3 key findings →
Evidence: low
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Neurodegeneration in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) results from both gain of toxicity and loss of normal function of the RNA-binding protein TDP-43, but their mechanistic connection remains unclear. 3 key findings →
Evidence: low
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87 DLB patients (77.5 ± 7.2yo; 34.5 % females) were included. 4 key findings →
Evidence: low
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Cerebral amyloid angiopathy (CAA) is a common age-related disorder, a prominent comorbidity of Alzheimer disease (AD), and causes vascular cognitive impairment and dementia. 3 key findings →
Evidence: low
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We have shown that B6 and WSB genetic backgrounds are less susceptible to CAA compared to BXW, which develops robust CAA. 5 key findings →
Evidence: low
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This narrative review of Alzheimer's disease (AD) history, therapy and prevention shows that its conceptualization has changed three times over 100 years. 5 key findings →
Design: narrative review Evidence: low
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Mutations in the Integral membrane protein 2B (ITM2B) gene are linked to the development of familial British and Danish dementias, two relatively early-onset dementia disorders known also to be associated with Tau neurofibrillary tangles (NFTs). 2 key findings →
Evidence: moderate
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Perturbations in the metabolism of microtubule‐associated protein tau (tau) underlie the pathology of a broad array of dementias, including chronic traumatic encephalopathy, amyotrophic lateral sclerosis (ALS) with cognitive impairment (ALSci) and approximately half of the dementias associated with frontotemporal lobar degeneration. 2 key findings →
Evidence: low
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Chronic cerebral hypoperfusion induced by permanent unilateral common carotid artery occlusion in mice was recently found to induce an age-dependent formation of insoluble cytoplasmic TDP-43 aggregates reminiscent of pathological changes found in human vascular dementia. 2 key findings →
Evidence: low
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Vascular dementia is a common cognitive disorder that is often triggered by neuroinflammatory responses caused by cerebrovascular injury, which further exacerbates the progression of the disease. 1 key finding →
Evidence: high
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Alzheimer's disease is the leading cause of dementia worldwide. 1 key finding →
Evidence: low
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The data suggest that TNFSF10 system-targeted treatment effectively restrain overshooting central and peripheral inflammation by rebalancing the overall immune response, mitigating the progression of AD pathology. 4 key findings →
Evidence: low
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Our results show that genotype, AOF, and sex contributed to AD-like pathology. 5 key findings →
Evidence: low
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Alzheimer's disease (AD) is a multifactorial disorder associated with neuroinflammation, elevated oxidative stress, lipid alterations as well as amyloid-deposits and the formation of neurofibrillary tangles. 5 key findings →
Evidence: low
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Dietary supplement silver nanoparticles have recently drawn attention following reports of hazards associated with long-term use. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD), the most common form of dementia, is marked by cognitive decline and amyloid-beta (Aβ) plaque deposition in the brain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Emerging evidence highlights the central role of peripheral immune-metabolic regulation in the pathogenesis of Alzheimer's disease and related dementias (ADRD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer’s disease (AD), the leading cause of dementia, is a multifaceted neurodegenerative disorder characterized by amyloid-beta (Aβ) aggregation, tau pathology, and neuroinflammation. 5 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 →