27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The relationship of microglia and astrocytes to deposits of beta-amyloid protein (BAP) was studied in Alzheimer's disease by immunohistochemistry. 4 key findings →
Evidence: low
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Alzheimer disease (AD) accounts for 60-70% of dementia cases. 4 key findings →
Evidence: low
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Microglial cells closely interact with senile plaques in Alzheimer's disease and acquire the morphological appearance of an activated phenotype. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
It has become apparent that the intestinal microbiota orchestrates important aspects of our metabolism, immunity, and development. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The symptoms of Alzheimer disease reflect a loss of neural circuit integrity in the brain, but neurons do not work in isolation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are neurodegenerative diseases that overlap in their clinical presentation, pathology and genetics, and likely represent a spectrum of one underlying disease. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is an intractable progressive neurodegenerative disease characterized by cognitive decline and dementia. 4 key findings →
Evidence: low
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Disrupted hippocampal performance underlies psychiatric comorbidities and cognitive impairments in patients with neurodegenerative disorders. 4 key findings →
Evidence: low
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Neuroinflammation may be involved in the pathophysiology of Parkinson's disease (PD) and specifically in non-motor symptoms such as depression, fatigue and cognitive impairment. 4 key findings →
Participants: 87 Evidence: low
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Polyphenols, naturally occurring phytonutrients found in plant-based foods, have attracted significant attention for their potential therapeutic effects in neurological diseases and neuroinflammation. 3 key findings →
Evidence: low
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Our meta-analyses confirmed significantly lower CSF TAU levels in DLB and CSF SYUA levels in PDD, when compared to Alzheimer's disease. 4 key findings →
Design: systematic review Evidence: high
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This study summarizes the existing literature on TSPO expression in specific regions of the brain in patients with dementia, and also provides some preliminary evidence on the possible association between neuroinflammation and dementia. 5 key findings →
Design: meta-analysis Evidence: high
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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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Vascular cognitive impairment risk factors include stroke, hypertension, diabetes and atherosclerosis. 1 key finding →
Design: meta-analysis Evidence: low
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1. Of the neurodegenerative diseases that cause dementia, Alzheimer's disease (AD) is the most common. 2 key findings →
Design: longitudinal study Evidence: moderate
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Inflammation is a physiological process that repairs tissues in response to endogenous or exogenous aggressions. 2 key findings →
Design: cohort study Evidence: moderate
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The blood-brain barrier (BBB) is a diffusion barrier, which impedes influx of most compounds from blood to brain. 4 key findings →
Evidence: low
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Microglia, the resident macrophages of the CNS, are exquisitely sensitive to brain injury and disease, altering their morphology and phenotype to adopt a so-called activated state in response to pathophysiological brain insults. 4 key findings →
Evidence: low
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Cultured brain cells are capable of generating many molecules associated with inflammatory and immune functions. 4 key findings →
Evidence: low
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Disturbances along the brain-gut-microbiota axis may significantly contribute to the pathogenesis of neurodegenerative disorders. 4 key findings →
Evidence: low
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Accumulating evidence suggests that neurodegeneration induced by pathogenic proteins depends on contributions from surrounding glia. 4 key findings →
Evidence: low
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Type 2 diabetes is a risk factor for Alzheimer's disease, most likely linked to an impairment of insulin signaling in the brain. 4 key findings →
Evidence: low
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The past 20 years have seen a gain in knowledge on microglia biology and microglia functions in disease that exceeds the expectations formulated when the microglia "immune network" was introduced. 4 key findings →
Evidence: low
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The presence of tangles of abnormally phosphorylated tau is a characteristic of Alzheimer's disease (AD), and the loss of synapses correlates with the degree of dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the most common dementia in the elderly. 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 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 →