The implication of gut microbiota in the control of brain functions in health and disease is a novel, currently emerging concept. 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.
The implication of gut microbiota in the control of brain functions in health and disease is a novel, currently emerging concept. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The potential neuroprotective effects of antidiabetic treatments have been largely assessed in Alzheimer's disease (AD) and AD-like dementia models, with or without metabolic disorders. 1 key finding →
Design: systematic review Participants: 405 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The findings underscore the potential of integrating physical exercise into comprehensive AD management strategies. 4 key findings →
Design: systematic review Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
NE3107 was associated with clinician-rated improvements in cerebral blood flow and functional connectivity within the brain. 3 key findings →
Design: clinical trial Participants: 17 Evidence: low
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Cerebrovascular diseases are well established causes of cognitive impairment. 5 key findings →
Design: systematic review Evidence: high
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Adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) is a progressive degenerative white matter disorder. 1 key finding →
Design: systematic review Evidence: high
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Microglial cells represent the immune system of the mammalian brain and therefore are critically involved in various injuries and diseases.
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Proliferation and activation of microglia in the brain, concentrated around amyloid plaques, is a prominent feature of Alzheimer's disease (AD).
Full summary, score breakdown and related studies → Original source Free full text
The role of microglial cells in the pathogenesis of Alzheimer's disease (AD) neurodegeneration is unknown. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Astrocytes are abundant glial cells in the central nervous system (CNS) that perform diverse functions in health and disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Inflammation and immune mechanisms are crucially involved in the pathophysiology of the development, acute damage cascades, and chronic course after ischemic stroke. 4 key findings →
Evidence: low
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Neuronal and glial cell interaction is essential for synaptic homeostasis and may be affected in Alzheimer's disease (AD). 4 key findings →
Participants: 36 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The chronic effects of repetitive head impacts (RHI) on the development of neuroinflammation and its relationship to chronic traumatic encephalopathy (CTE) are unknown. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Genetic risk factors for Alzheimer's disease imply that inflammation plays a causal role in development of the disease. 4 key findings →
Participants: 299 Evidence: low
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Alzheimer's disease (AD) is the leading cause of dementia and is characterized by progressive amyloid accumulation followed by tau-mediated neurodegeneration. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
PD may be a modifiable risk factor for AD, and periodontal interventions could contribute to AD prevention and management. 2 key findings →
Design: case-control study Participants: 52 Evidence: moderate
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Alzheimer's disease (AD), a heterogeneous neurodegenerative disorder, is the most common cause of dementia accounting for an estimated 60-80% of cases. 1 key finding →
Design: systematic review Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Here we describe results of a Phase 2a study of a promising new drug candidate that significantly reversed all measured biomarkers of Alzheimer's disease, neurodegeneration and neuroinflammation. 5 key findings →
Design: open-label trial Participants: 13 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Full summary, score breakdown and related studies → Original source Free full text
This longitudinal study sought to determine whether the 18 kDa translocator protein (TSPO), a marker of neuroinflammation, increases over time in Alzheimer's disease. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Increased CSF NFL indicates ongoing axonal injury in many neuroasymptomatic patients. 2 key findings →
Design: cross-sectional Participants: 200 Evidence: low
Full summary, score breakdown and related studies → Original source
Both acute and chronic systemic inflammation, associated with increases in serum tumor necrosis factor alpha, is associated with an increase in cognitive decline in Alzheimer disease. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
In Alzheimer disease (AD), amyloid β peptide (Aβ) accumulates in plaques in the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The pathogenesis of human immunodeficiency virus (HIV)-associated dementia is unclear, and the underlying pathological substrate has been a matter of debate. 4 key findings →
Participants: 51 Evidence: low
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Systemic infection and drugs with anticholinergic effects are well-recognised and prevalent risk factors for delirium in elderly people. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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 →