27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
AD is a neurodegenerative disease, and its frequency is often reported to be higher for women than men: almost two-thirds of patients with AD are women. 4 key findings →
Evidence: low
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The increasing availability of single-cell data revolutionizes the understanding of biological mechanisms at cellular resolution. 4 key findings →
Evidence: moderate
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Alzheimer's disease (AD) is currently untreatable, and therapeutic strategies aimed to slow cognitive decline have not yet been successful. 4 key findings →
Evidence: low
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Microglia are central players in brain innate immunity and have been the subject of extensive research in Alzheimer's disease (AD). 3 key findings →
Evidence: low
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Accumulation of mononuclear phagocytes [monocytes, macrophages, and dendritic cells (DCs)] in the vessel wall is a hallmark of atherosclerosis. 4 key findings →
Evidence: low
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Identifying factors underlying resistance to immune checkpoint therapy (ICT) is still challenging. 4 key findings →
Evidence: low
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Recent evidence suggests that rare genetic variants within the TREM2 gene are associated with increased risk of Alzheimer's disease. 4 key findings →
Evidence: moderate
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Triggering receptor expressed on myeloid cells 2 (TREM2) sustains microglia response to brain injury stimuli including apoptotic cells, myelin damage, and amyloid β (Aβ). 4 key findings →
Evidence: low
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Proteomic studies for Alzheimer's disease (AD) are instrumental in identifying AD pathways but often focus on single tissues and sporadic AD cases. 4 key findings →
Evidence: low
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Multiple sclerosis (MS) is a chronic inflammatory disease affecting the central nervous system (CNS). 4 key findings →
Design: longitudinal study Evidence: moderate
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Triggering receptor expressed on myeloid cells 2 (TREM2) is a transmembrane protein that is predominantly expressed by microglia in the brain. 4 key findings →
Evidence: low
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Candidate cis-regulatory elements (cCREs) in microglia demonstrate the most substantial enrichment for Alzheimer's disease (AD) heritability compared to other brain cell types. 4 key findings →
Evidence: low
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BACKGROUNDSoluble triggering receptor expressed on myeloid cells 2 (sTREM2) plays an important role in the clearance of pathological amyloid-β (Aβ) in Alzheimer's disease (AD). 4 key findings →
Evidence: moderate
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The detection of genetic loci associated with Alzheimer's disease (AD) requires large numbers of cases and controls because variant effect sizes are mostly small. 4 key findings →
Design: case-control study Evidence: moderate
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We analyzed CSF concentrations of neurogranin, β-amyloid (Aβ42), phosphorylated tau (p-tau), and total tau (t-tau) among 132 neurologically normal older adults (mean 64.5, range 55-85), along with bilateral hippocampal volumes and a measure of episodic memory (Auditory Verbal Learning Test, delayed recall). 4 key findings →
Evidence: low
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Hyperhomocysteinemia is a risk factor for cognitive decline and dementia, including Alzheimer disease (AD). 4 key findings →
Design: cross-sectional Participants: 72 Evidence: low
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The primary cohort included 91 AAs and 868 NHWs. 4 key findings →
Participants: 91 Evidence: moderate
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We investigated whether specific SLEs are associated with AD pathology and neurodegeneration and how these associations differ by gender and education. 4 key findings →
Design: cross-sectional Evidence: moderate
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In vitro and animal studies have suggested that inoculation with herpes simplex virus 1 (HSV-1) can lead to amyloid deposits, hyperphosphorylation of tau, and/or neuronal loss. 4 key findings →
Participants: 58 Evidence: low
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Cerebral amyloid angiopathy (CAA) is driven by vascular Aβ (amyloid-beta) deposition, which can be detected as reduced Aβ species in cerebrospinal fluid (CSF). 4 key findings →
Design: cross-sectional Participants: 31 Evidence: low
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Diet can impact cognitive aging, but comprehensive data from human studies is lacking and the underlying biological mechanisms are still not fully understood. 4 key findings →
Design: cross-sectional Participants: 1,907 Evidence: low
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Early identification of Alzheimer's disease (AD) pathology is essential for timely intervention, particularly in primary care. 4 key findings →
Participants: 181 Evidence: moderate
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Prion disease and Alzheimer disease (AD) are common causes of rapidly progressive dementia (RPD). 4 key findings →
Design: systematic review Participants: 15 Evidence: high
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Sleep spindles (SPs) and slow oscillations (SOs) are linked to cognition and neurodegeneration; however, their relationship with CSF orexin concentrations in symptomatic AD has not been characterized. 4 key findings →
Design: cohort study Evidence: moderate
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In vivo biomarkers for detecting neuropathologies from repetitive head impacts (RHI), including chronic traumatic encephalopathy (CTE), are needed. 4 key findings →
Design: case-control study Participants: 231 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.
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 →