Loss-of-function TREM2 mutations strongly increase Alzheimer's disease (AD) risk. 4 key findings →
Evidence: low
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.
Loss-of-function TREM2 mutations strongly increase Alzheimer's disease (AD) risk. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
APOE and Trem2 are major genetic risk factors for Alzheimer's disease (AD), but how they affect microglia response to Aβ remains unclear. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
TREM2 is a pattern recognition receptor, expressed on microglia and myeloid cells, detecting lipids and Aβ and inducing an innate immune response. 4 key findings →
Evidence: low
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Ovarian carcinomas (OCs) are poorly immunogenic and immune checkpoint inhibitors (ICIs) have offered a modest benefit. 4 key findings →
Participants: 312 Evidence: low
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Mild cognitive impairment (MCI) detection using magnetic resonance image (MRI), plays a crucial role in the treatment of dementia disease at an early stage. 4 key findings →
Evidence: low
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Previous research has described distinct subtypes of Alzheimer's disease (AD) based on the differences in regional patterns of brain atrophy on MRI. 4 key findings →
Evidence: low
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Identifying biomarkers associated with Alzheimer's disease (AD) progression may enable patient enrichment and improve clinical trial designs. 4 key findings →
Participants: 19 Evidence: moderate
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While insulin-like growth factor-1 (IGF-1) is a well-established modulator of aging and longevity in model organisms, its role in humans has been controversial. 4 key findings →
Participants: 440,185 Evidence: low
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White matter hyperintensities (WMH) are among the most common radiological abnormalities in the ageing population and an established risk factor for stroke and dementia. 4 key findings →
Evidence: low
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We show that m 6 A modification displays temporal and spatial dynamics during neurodevelopment and aging. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is a major contributor of dementia leading to the degeneration of neurons in the brain with major symptoms like loss of memory and learning. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is a complex neurodegenerative disease in the elderly and the most common cause of human dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Microglial-mediated neuroinflammation plays an important role in vascular dementia, and modulating neuroinflammation has emerged as a promising treatment target. 4 key findings →
Evidence: low
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Dysfunction of immune and vascular systems has been implicated in aging and Alzheimer disease; however, their interrelatedness remains poorly understood. 4 key findings →
Evidence: low
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These results indicate lipid droplet accumulation occurs in human DAM xMGs in AD, but is reduced in TREM2-R47H DAM xMGs, as it occurs secondary to TREM2-mediated changes in plaque proximity and reactivity. 5 key findings →
Evidence: low
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SiD represents a new resource for promoting safety among people with dementia, and high acceptability was achieved in a pilot trial. 2 key findings →
Design: clinical trial Participants: 203 Evidence: high
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Vascular cognitive impairment (VCI) is predominately caused by vascular risk factors and cerebrovascular disease. 2 key findings →
Evidence: low
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Clinical Alzheimer's disease (AD) trials currently face a critical shortfall of thousands of eligible participants, which inflates the duration and cost of the clinical study as well as threatens the scientific merit of promising clinical interventions. 2 key findings →
Design: narrative review Evidence: low
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Dementia is the clinical syndrome characterized by progressive loss of cognitive and emotional abilities to a degree severe enough to interfere with daily functioning. 1 key finding →
Evidence: low
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The diversity of cognitive deficits and neuropathological processes associated with dementias has encouraged divergence in pathophysiological explanations of disease. 1 key finding →
Evidence: low
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The dCDT is able to operationally define graphomotor output that cannot be measured using traditional paper and pencil test administration in older health controls and participants with dementia. 4 key findings →
Participants: 175 Evidence: low
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Oculomotor behavior can provide insight into the integrity of widespread cortical networks, which may contribute to the differential diagnosis between Alzheimer's disease and frontotemporal dementia. 2 key findings →
Participants: 93 Evidence: low
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The alteration of the insulin-signaling/mTOR pathways represents an early event in DS brain and likely contributes to the cerebral dysfunction and intellectual disability observed in this unique population. 1 key finding →
Participants: 17 Evidence: low
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Transcranial magnetic stimulation (TMS) is a powerful tool to probe in vivo brain circuits, as it allows to assess several cortical properties such asexcitability, plasticity and connectivity in humans. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Applying an integrative multi-omics approach we report novel molecular and pathways alterations associated with AD pathology. 5 key findings →
Evidence: moderate
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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 →