30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Recent findings from single-cell transcriptomic studies prompted us to revisit the role of plaque foamy macrophages in the pathogenesis of atherosclerosis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Human genetic studies have linked rare coding variants in microglial genes, such as TREM2, and more recently PLCG2 to Alzheimer's disease (AD) pathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Calcium dysregulation ("Calcium Hypothesis") is an early and critical event in Alzheimer's and other neurodegenerative diseases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings support the therapeutic potential of modulating, rather than suppressing, neuroinflammation in Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Accumulating evidence indicates that Alzheimer disease (AD) is caused by dysregulated microglial phagocytosis. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
During aging, several tissues and biological systems undergo a progressive decline in function, leading to age-associated diseases such as neurodegenerative, inflammatory, metabolic, and cardiovascular diseases and cancer. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Triggering Receptor Expressed in Myeloid Cells 2 (TREM2) is a pattern recognition receptor on myeloid cells, and is upregulated on microglia surrounding amyloid plaques in Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
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
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
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
10 of the 8,313 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.
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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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 (3.4% 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 →