The INTε4+ group did not seem markedly more responsive to the guidance than the other groups. 2 key findings →
Participants: 33 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
29,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The INTε4+ group did not seem markedly more responsive to the guidance than the other groups. 2 key findings →
Participants: 33 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Recent research has shown an increased rate of conversion to dementia in subjects with mild cognitive impairment (MCI) compared to controls. 5 key findings →
Participants: 13 Evidence: low
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Alzheimer's disease (AD) is characterized by a robust inflammatory response elicited by the accumulation and subsequent deposition of amyloid (Aβ) within the brain. 4 key findings →
Evidence: low
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Microglia-specific genetic variants are enriched in several neurodegenerative diseases, including Alzheimer's disease (AD), implicating a central role for alterations of the innate immune system in the disease etiology. 4 key findings →
Evidence: low
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The global prevalence of dementia is increasing. 1 key finding →
Evidence: low
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Our results elucidate the characteristics and genetic associations of p‐tau217 in a population‐based setting. 4 key findings →
Participants: 697 Evidence: low
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Protein kinase B (PKB) is an important intermediate in the phosphatidylinositol-3 kinase signaling cascade that acts to phosphorylate glycogen synthase kinase-3 (GSK-3) at its serine 9 residue, thereby inactivating it. 4 key findings →
Evidence: low
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Individuals with Down's syndrome (DS) develop early Alzheimer's disease (AD) with β-amyloid (Aβ) plaque pathology. 4 key findings →
Participants: 12 Evidence: low
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The AddNeuroMed and ADNI cohorts were combined giving a total of 329 healthy controls, 421 mild cognitive impairment patients, and 286 Alzheimer's disease (AD) patients. 4 key findings →
Participants: 329 Evidence: low
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The role of microglia recruited from bone marrow (BM) into the CNS during the progression of Alzheimer's disease (AD) is poorly understood. 4 key findings →
Evidence: low
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BackgroundDifferentiating neurodegenerative diseases can be difficult in the clinical setting. 2 key findings →
Participants: 2,751 Evidence: low
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Prevalent LB- and AD-related neurodegenerative pathologies affect a significant proportion of iNPH patients and contribute to cognitive decline (both) and motor impairment (only LB pathology) but do not significantly influence the surgical outcome at 6 months. 5 key findings →
Evidence: moderate
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The Alzheimer's Disease Sequencing Project (ADSP) undertook whole exome sequencing in 5,740 late-onset Alzheimer disease (AD) cases and 5,096 cognitively normal controls primarily of European ancestry (EA), among whom 218 cases and 177 controls were Caribbean Hispanic (CH). 2 key findings →
Evidence: low
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NPS are common even in the early stages of AD. 3 key findings →
Evidence: low
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Rey's Auditory Verbal Learning Test (RAVLT) is a powerful neuropsychological tool for testing episodic memory, which is widely used for the cognitive assessment in dementia and pre-dementia conditions. 2 key findings →
Evidence: low
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Chronic psychosocial stress is increasingly recognized as a risk factor for late-onset Alzheimer's disease (LOAD) and associated cognitive deficits. 4 key findings →
Evidence: low
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Neurodegenerative processes of various types of dementia start years before symptoms, but the presence of a "neural reserve", which continuously feeds and supports neuroplastic mechanisms, helps the aging brain to preserve most of its functions within the "normality" frame. 1 key finding →
Evidence: low
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The concept of mild cognitive impairment (MCI) has been proposed to represent a transitional stage between normal aging and dementia. 1 key finding →
Participants: 60 Evidence: low
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Analysis of the genotyping data revealed that the TMEM106B locus consists of four major haplotypes: HA/Ha (covering the coding region), and HB/Hb (covering the upstream regulatory region). 5 key findings →
Participants: 182 Evidence: low
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The total number of new diagnoses of dementia with a vascular component or vascular alone was 202, with 20 cases attributable to pure VD. 5 key findings →
Evidence: low
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Biallelic loss-of-function variants in TYROBP and TREM2 cause autosomal recessive presenile dementia with bone cysts known as Nasu-Hakola disease (NHD, alternatively polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy, PLOSL). 3 key findings →
Evidence: low
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In this study, we have assessed the expression and splicing status of genes involved in the pathogenesis or affecting the risk of Alzheimer's disease (AD) in the postmortem inferior temporal cortex samples obtained from 60 subjects with varying degree of AD-related neurofibrillary pathology. 4 key findings →
Participants: 60 Evidence: low
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We measured the activities of choline acetyltransferase (ChAT) in the post mortem frontal cortex in 32 Alzheimer's disease (AD) patients with different apolipoprotein E (apoE) genotypes. 4 key findings →
Evidence: low
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We found 129 articles that applied transfer learning to MR brain imaging tasks. 5 key findings →
Evidence: low
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A population of >6 million people worldwide at high risk of Alzheimer’s disease (AD) are those with Down Syndrome (DS, caused by trisomy 21 (T21)), 70% of whom develop dementia during lifetime, caused by an extra copy of β-amyloid-(Aβ)-precursor-protein gene. 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 29,380 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 29,380 records, built mostly from automated pulls of Europe PMC (63.3% of the library) and OpenAlex (17.3%), 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.
1,037 records (3.5% of the library) are not peer-reviewed — 964 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 →