Alzheimer's disease (AD) has been genetically and pathologically associated with neuroinflammation. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease (AD) has been genetically and pathologically associated with neuroinflammation. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
It has become increasingly evident that neuroinflammation plays a critical role in the pathophysiology of Alzheimer's disease (AD) and other neurodegenerative disorders. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Metabolic changes play a crucial role in determining the status and function of macrophages, but how lipid reprogramming in macrophages contributes to tumor progression is not yet fully understood. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We examined the effect of chronic high fat diet (HFD) on amyloid deposition and cognition of 12-months old APP23 mice, and correlated the phenotype to brain transcriptome and lipidome. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Chronic psychological stress is one of the most important triggers and environmental risk factors for neuropsychiatric disorders. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Microglia, the brain's principal immune cells, have been implicated in the pathogenesis of Alzheimer's disease (AD), a condition shown to affect more females than males. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a late-onset dementia characterized by the deposition of amyloid plaques and formation of neurofibrillary tangles (NFTs) which lead to neuronal loss and cognitive deficits. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Animal work investigating the consequences of maternal high-fat diet (mHFD) revealed in the offspring a maternal immune activation (MIA) phenotype associated with increased inflammatory signals. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Nasu-hakola disease (NHD) is a rare disease characterized by bone cysts and fractures, frontal lobe syndrome, and progressive presenile dementia. 4 key findings →
Evidence: low
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Murine microglia expressing the Alzheimer's disease-linked TREM2 R47H mutation display variable decrease in phagocytosis, while impaired phagocytosis is reported following loss of TREM2. 4 key findings →
Evidence: low
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The classical amyloid cascade model for Alzheimer's disease (AD) has been challenged by several findings. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In this review, we focus on the emerging roles of microglia in the brain, with particular attention to synaptic plasticity in health and disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Microglia plays crucial roles in Alzheimer's disease (AD) development. 4 key findings →
Evidence: low
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Microglia are a specialized type of neuroimmune cells that undergo morphological and molecular changes through multiple signaling pathways in response to pathological protein aggregates, neuronal death, tissue injury, or infections. 4 key findings →
Evidence: low
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Alzheimer's disease (AD), Parkinson's disease (PD), frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS), Huntington's disease (HD), and prion diseases have a certain degree of clinical, pathological, and molecular overlapping. 4 key findings →
Evidence: moderate
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Alzheimer disease (AD) is multi-factorial and heterogeneous. 4 key findings →
Evidence: low
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The microtubule-associated tau protein abnormally phosphorylated at threonine 231 (p-tau231) has been investigated as a potential marker of Alzheimer disease. 4 key findings →
Participants: 22 Evidence: low
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Protein kinase B (PKB) is an important intermediate in the phosphatidylinositol-3 kinase signaling cascade that acts to phosphorylate glycogen synthase kinase-3 (GSK-3) at its serine 9 residue, thereby inactivating it. 4 key findings →
Evidence: low
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The purpose of this study was to investigate the potential relationships between cerebrospinal fluid (CSF) measurements of beta-amyloid-1-42 (Abeta(1-42)) and total tau to (11)C-Pittsburgh compound B ((11)C-PiB) and 2-(1-{6-[(2-(18)F-fluoroethyl)(methyl)amino]-2-naphthyl}ethylidene) malononitrile ((18)F-FDDNP) binding as measured using PET. 4 key findings →
Participants: 37 Evidence: low
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Therapies designed to decrease the level of SOD1 are currently in a clinical trial for patients with superoxide dismutase (SOD1)-linked familial amyotrophic lateral sclerosis (ALS). 4 key findings →
Evidence: low
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Individuals with Down's syndrome (DS) develop early Alzheimer's disease (AD) with β-amyloid (Aβ) plaque pathology. 4 key findings →
Participants: 12 Evidence: low
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One-hundred nineteen individuals with a family history of AD (Presymptomatic Evaluation of Experimental or Novel Treatments of Alzheimer's Disease [PREVENT-AD] cohort, mean age 67 ± 5 years) underwent tau-PET ([ 18 F]FTP), β-amyloid (Aβ)-PET ([ 18 F]NAV4694 [NAV]), and cognitive assessment. 4 key findings →
Evidence: moderate
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Biomarkers are needed to improve the sensitivity and accuracy of diagnosis, and also prognosis, in individuals with early Alzheimer disease (AD). 4 key findings →
Design: longitudinal study Evidence: moderate
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Neuraminidase 1 (NEU1) cleaves terminal sialic acids from sialoglycoproteins in endolysosomes and at the plasma membrane. 4 key findings →
Evidence: low
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Concentrations of phosphorylated tau181, total tau (t-tau), and β-amyloid in the CSF were measured in 3 groups: 22 former professional athletes with multiple concussions (mean ± SD age 55.9 ± 12.2 years), 5 healthy controls (age 57.4 ± 5.2 years), and 12 participants (age 60.0 ± 6.6 years) diagnosed with Alzheimer disease (AD). 4 key findings →
Participants: 12 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.
1,034 records (3.7% 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 →