Neurodegenerative diseases likely share common underlying pathobiology. 5 key findings →
Participants: 82,337 Evidence: low
Full summary, score breakdown and related studies → Original source
30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Neurodegenerative diseases likely share common underlying pathobiology. 5 key findings →
Participants: 82,337 Evidence: low
Full summary, score breakdown and related studies → Original source
ECT-induced neuroplasticity in the hippocampus and amygdala relates to improved clinical response and is pronounced in regions with prominent connections to ventromedial prefrontal cortex and other limbic structures. 2 key findings →
Design: cross-sectional Participants: 43 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Increasing evidence has shown the potential value of plasma biomarkers in Alzheimer's disease diagnosis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent genome-wide association studies linked variants in TREM2 to a strong increase in the odds of developing Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Identifying factors underlying resistance to immune checkpoint therapy (ICT) is still challenging. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Bile acids (BAs) may contribute to dementia by regulating neuroinflammation and influencing gut-brain axis signaling, especially in Alzheimer's disease (AD). 3 key findings →
Design: cross-sectional Evidence: moderate
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CAARS has the potential to predict CAA severity; however, its clinical utility should be evaluated in follow-up studies. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our results confirmed the diagnostic performance of individual plasma biomarkers Aβ42/Aβ40, p-tau181, NfL, and GFAP in Chinese dementia patients and noted that a combination of these biomarkers may be more accurate in identifying FTD/PSP patients and distinguishing AD from non-AD dementia. 2 key findings →
Participants: 92 Evidence: moderate
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Individuals with SCD had an altered cortical surface area, and APOE genotype and anxiety symptoms are modified factors on the cortical surface area decrease in SCD. 4 key findings →
Participants: 65 Evidence: moderate
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Patients with AD and MCI have decreased microbial diversity, and changes in gut microbiota could be detected for early detection of AD. 1 key finding →
Evidence: low
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Computational anatomy methods are now widely used in clinical neuroimaging to map the profile of disease effects on the brain and its clinical correlates. 1 key finding →
Participants: 490 Evidence: low
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Mitochondrial dysfunction is a prominent feature of Alzheimer disease but the underlying mechanism is unclear. 4 key findings →
Evidence: low
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Like acetylcholinesterase, butyrylcholinesterase (BChE) inactivates the neurotransmitter acetylcholine (ACh) and is hence a viable therapeutic target in Alzheimer's disease, which is characterized by a cholinergic deficit. 4 key findings →
Evidence: low
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Genome-wide association studies have identified rare variants of the gene that encodes triggering receptor expressed on myeloid cells 2 (TREM2) - an immune receptor that is found in brain microglia - as risk factors for non-familial Alzheimer disease (AD). 2 key findings →
Evidence: low
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During lecanemab treatment for AD, it is essential to fully understand the mechanisms, imaging characteristics, and management strategies of ARIA. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Accurate and early diagnosis of Alzheimer's disease (AD) plays important role for patient care and development of future treatment. 1 key finding →
Participants: 397 Evidence: low
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We investigated the genetic overlap between Alzheimer's disease (AD) and Parkinson's disease (PD). 3 key findings →
Participants: 89 Evidence: low
Full summary, score breakdown and related studies → Original source
Our study suggested that TREM2 (rs75932628-T) was rare in Chinese Han population. 4 key findings →
Design: case-control study Evidence: moderate
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Interest in understanding the roles of white matter (WM) inflammation and damage in the pathophysiology of Alzheimer disease (AD) has been growing significantly in recent years. 5 key findings →
Participants: 200 Evidence: low
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Immune checkpoint inhibitors targeting programmed cell death protein 1, programmed death-ligand 1, and cytotoxic T-lymphocyte-associated protein 4 provide deep and durable treatment responses which have revolutionized oncology. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) and cancer are among the most devastating diseases worldwide. 2 key findings →
Evidence: early
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One of the pathological hallmarks of Alzheimer disease is the accumulation of amyloid plaques in the extracellular space in the brain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Sepsis-induced cardiomyopathy (SICM) is common in septic patients with a high mortality and is characterized by an abnormal immune response. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Triggering receptor expressed on myeloid cells 2 (TREM2) has been shown with a neuroprotective function against inflammation and neuronal injury in Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neuroinflammation is one of the most important processes in secondary injury after traumatic brain injury (TBI). 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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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 →
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