Accumulating evidence has demonstrated the involvement of B cells in neuroinflammation and neuroregeneration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
As individuals age, microglia, the resident immune cells of the central nervous system (CNS), become less effective at preserving brain circuits. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia are brain-dwelling macrophages and major parts of the neuroimmune system that broadly contribute to brain development, homeostasis, ageing and injury repair in the central nervous system (CNS). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Sleep disturbances not only deteriorate Alzheimer's disease (AD) progress by affecting cognitive states but also accelerate the neuropathological changes of AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Epidemiological studies have found that heavy alcohol use is associated with increased risk for Alzheimer's disease (AD), with frequent drinking earlier in adulthood increasing risk. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The microtubule-associated protein tau has been implicated in the pathogenesis of Alzheimer's disease (AD) and other neurodegenerative disorders. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
Neuronal expression of familial Alzheimer's disease-mutant human amyloid precursor protein (hAPP) and hAPP-derived amyloid-beta (Abeta) peptides causes synaptic dysfunction, inflammation and abnormal cerebrovascular tone in transgenic mice. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Brain infiltration of peripheral immune cells and their interactions with brain-resident cells may contribute to Alzheimer's disease (AD) pathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Astrocytes become reactive in response to insults to the central nervous system by adopting context-specific cellular signatures and outputs, but a systematic understanding of the underlying molecular mechanisms is lacking. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Selective neurodegeneration is a critical causal factor in Alzheimer's disease (AD); however, the mechanisms that lead some neurons to perish, whereas others remain resilient, are unknown. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
Senescent cells contribute to pathology and dysfunction in animal models 1 . 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is an age-related disease pathologically defined by the deposition of amyloid plaques and neurofibrillary tangles in the brain parenchyma. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
These results suggest that multi-factor proteomic pattern analysis of the CSF may provide a means to diagnose and assess AD. 4 key findings →
Participants: 43 Evidence: low
Full summary, score breakdown and related studies → Original source
We used a combined proteomic and functional biochemical approach to determine the overall impact of 17beta-estradiol (E2) on mitochondrial protein expression and function. 3 key findings →
Participants: 66 Evidence: low
Full summary, score breakdown and related studies → Original source
Aging induces molecular, cellular and functional changes in the adult brain that drive cognitive decline and increase vulnerability to dementia-related neurodegenerative diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Human middle temporal gyrus (MTG) is a vulnerable brain region in early Alzheimer's disease (AD), but little is known about the molecular mechanisms underlying this regional vulnerability. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Metzincin metalloproteases have major roles in intercellular communication by modulating the function of membrane proteins. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings demonstrate that fibrillar Aβ in microglia is associated with lipid dyshomeostasis consistent with lysosomal dysfunction and foam cell phenotypes as well as profound immuno-metabolic perturbations, opening new avenues to further investigate metabolic pathways at play in microglia responding to AD-relevant pathogenesis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
Apolipoprotein E4 (APOE4) is the strongest known genetic risk factor for late-onset Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We showed that ultrasound resulted in an almost 5-fold increase in the exosome release from human astrocytes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
We find that as with APP, endosomal trafficking of GLUA1 and TRKB is impaired by loss of SORL1. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Blood protein extravasation through a disrupted blood-brain barrier and innate immune activation are hallmarks of neurological diseases and emerging therapeutic targets. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
Cerebrovascular disease underpins vascular dementia (VaD), but structural and functional changes to the cerebral vasculature contribute to disease pathology and cognitive decline in Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
The peripheral immune system is thought to affect the pathology of the central nervous system in Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia play a critical role in brain homeostasis and disease progression. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 8,203 studies in this tag that have a study page, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- The dual role of astrocyte activation and reactive gliosis
- Okadaic acid induces early changes in microtubule-associated protein 2 and tau phosphorylation prior to neurodegeneration in cultured cortical neurons
- Tunicamycin impairs olfactory learning and synaptic plasticity in the olfactory bulb
- Biomarkers for insulin resistance and inflammation and the risk for all-cause dementia and alzheimer disease: results from the Framingham Heart Study
- Ex vivo expanded human regulatory T cells modify neuroinflammation in a preclinical model of Alzheimer's disease
- The exosome of adipose-derived stem cells reduces β-amyloid pathology and apoptosis of neuronal cells derived from the transgenic mouse model of Alzheimer's disease
- Morphological and biochemical analyses of amyloid plaque core proteins purified from Alzheimer disease brain tissue
- Age-related hearing loss: prevention of threshold declines, cell loss and apoptosis in spiral ganglion neurons
- Alzheimer precursor protein interaction with the Nogo-66 receptor reduces amyloid-beta plaque deposition
- Human multiscale transcriptomics identifies the NLRP3 inflammasome as a convergent druggable target in Alzheimer’s disease: validation with dimethyl itaconate in 5xFAD mice
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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 29,780 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.
What this library is — and isn't
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), 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.
1,037 records (3.5% of the library) are not peer-reviewed — 964 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 →