30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Neuroinflammation is a hallmark of Alzheimer’s disease (AD); however, which neuroinflammatory effectors are consistently altered across independent human cohorts, brain regions, and microglial states—and can be engaged by available compounds—remains incompletely defined. 4 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Scalable and accessible biomarkers of neurofibrillary tangle pathology are needed for Alzheimer’s disease prognosis, diagnosis and monitoring. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
While tau plays a role in regulating neuronal network excitability, a process thought to be dysregulated in Alzheimer’s disease (AD), the molecular mechanisms linking tau and hyperexcitability remain unclear. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The GABA B receptor is a central regulator of neuronal transmission and excitability by pre- and postsynaptic mechanisms. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Quantitative analysis of dendritic spine morphology is central to understanding synaptic function and its disruption in neurological disease, yet reliable measurement depends on accurate segmentation of spines from fluorescence microscopy images — a task still limited by faint or discontinuous spine necks and by tools that require extensive manual correction. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent work has highlighted the importance of core Hippo pathway kinases in cycling cells. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
ABCA7-KO iMGs were deficient for proteins involved in lysosome function, measured by down-regulated lysosomal proteomic signatures, as well as reduced DQ-BSA activity and reduced LAMP1+ area. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Synapse loss occurs early in prion disease, yet the intracellular signaling driving this dysregulation remains poorly understood. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mutations in GRN and C9orf72 are common causes of frontotemporal dementia (FTD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Synapse loss is the strongest pathological correlate of cognitive decline in Alzheimer’s disease, yet the molecular basis of synaptic vulnerability across disease progression remains poorly understood. 2 key findings →
Participants: 67 Evidence: low
Full summary, score breakdown and related studies → Original source
Endosomal dysfunction is a presymptomatic hallmark of neurodegeneration. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
MicroRNAs (miRNAs) are implicated in Alzheimer's disease (AD), but research has focused on individual miRNAs and direct targets. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Physical exercise promotes systemic and neural adaptations that support healthy brain aging and may mitigate Alzheimer’s disease (AD) progression. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by the deposition of amyloid-beta (Aβ) and microtubule-associated protein tau (MAPT) neurofibrillary tangles in the brain; however, the molecular mechanisms underlying associated synaptic dysfunction remain unclear. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The apolipoprotein E ε4 (APOE4) allele is the strongest genetic risk factor for developing sporadic Alzheimer’s disease (AD), which accounts for the vast majority of AD cases. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Pathogenic tau oligomers are transmitted between neurons and non-neuronal cells and may contribute to cellular dysfunction in Alzheimer’s disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) exhibits an intricate and multifactorial pathogenesis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Defective mitophagy is emerging as a key contributor to Alzheimer’s disease (AD), but the neuronal pathways governing mitochondrial clearance and their contribution to disease progression remain poorly understood. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Auditory dysfunction can precede clinical dementia, but the molecular progression of Alzheimer disease (AD) pathology from the sensory periphery to auditory cortex remains poorly resolved. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mitochondrial dysfunction is a shared biological thread between terrestrial Alzheimer’s disease (AD) and in the unique stress environment of spaceflight, making mitochondrial pathophysiology a compelling target for comparative investigation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is characterized by a decline in neuronal proteostasis that favours the accumulation of misfolded proteins. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease involves progressive necroptosis of neurons, and the associated cognitive deficits can be mitigated by inhibiting cAMP-degrading phosphodiesterase 4D (PDE4D). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Most included studies were purely in vitro (n = 18); six combined in vitro and in vivo methods, and two used in vitro and in silico or ex vivo components. 1 key finding →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source
These findings demonstrate that Tau deletion induces an active, multilevel gain-of-resilience rather than passive resistance. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Whether the nodal vulnerability in dementia is solely represented by changes in cellular abundance or attrition of cellular transcriptomic landscape attribute to that transition in aging brain is yet to uncover with minutiae. 5 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 →