28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Biological systems are immensely complex, organized into a multi-scale hierarchy of functional units based on tightly regulated interactions between distinct molecules, cells, organs, and organisms. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia are the resident macrophages of the central nervous system (CNS) acting as the first line of defense in the brain by phagocytosing harmful pathogens and cellular debris. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Single-cell RNA sequencing (scRNA-seq) distinguishes cell types, states and lineages within the context of heterogeneous tissues. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The ability to investigate therapeutic interventions in animal models of neurodegenerative diseases depends on extensive characterization of the model(s) being used. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by extracellular aggregates of amyloid β peptides, intraneuronal tau aggregates, and neuronal death. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
DNA methyltransferase 1 (DNMT1) is crucial for maintenance of methylation, gene regulation and chromatin stability. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A common approach to understanding neurodegenerative disease is comparing gene expression in diseased versus healthy tissues. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Ferroptosis and neuroinflammation play crucial roles in Alzheimer's disease (AD) pathophysiology. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuroinflammation is a hallmark of many neurodegenerative diseases (NDs) and plays a fundamental role in mediating the onset and progression of disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
DNA methylation (5-methylcytosine [5mC]) is one of several epigenetic markers altered in Alzheimer's disease (AD) brain. 5 key findings →
Participants: 13 Evidence: low
Full summary, score breakdown and related studies → Original source
Classically, the following three morphological states of microglia have been defined: ramified, amoeboid and phagocytic. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cellular perturbations underlying Alzheimer's disease (AD) are primarily studied in human postmortem samples and model organisms. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Complex diseases are characterized by spatiotemporal cellular and molecular changes that may be difficult to comprehensively capture. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a complex neurodegenerative disease, perturbing neuronal and non-neuronal cell populations. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microtubule-associated protein tau is abnormally aggregated in neuronal and glial cells in a range of neurodegenerative diseases that are collectively referred to as tauopathies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau positron emission tomography ligands provide the novel possibility to image tau pathology in vivo However, little is known about how in vivo brain uptake of tau positron emission tomography ligands relates to tau aggregates observed post-mortem. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mean SUVRs were calculated for progressive supranuclear palsy, corticobasal degeneration, and neurofibrillary tangle Braak stage regions of interest, and these values were compared to SUVRs derived from young, non-autopsy, cognitively normal controls used as a standard for tau negativity. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mild behavioral impairment (MBI) is suggested as risk marker for neurodegenerative diseases, such as Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Abnormally phosphorylated tau, an indicator of Alzheimer's disease, accumulates in the first decades of life in the locus coeruleus (LC), the brain's main noradrenaline supply. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Both the replication of protein aggregates and their spreading throughout the brain are implicated in the progression of Alzheimer’s disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tauvid has been approved by the U.S. Food and Drug Administration (FDA) in 2020 for positron emission tomography (PET) imaging of adult patients with cognitive impairments undergoing evaluation for Alzheimer's disease (AD) based on tau pathology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Before any manifestations of cognitive or behavioral changes, there were differences in resting state connectivity in cognitively normal subjects with brain amyloid deposition, suggesting that early manifestation of Abeta toxicity can be detected using resting state fMRI. 3 key findings →
Participants: 35 Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid deposition is present in 20-50% of nondemented older adults yet the functional consequences remain unclear. 2 key findings →
Participants: 38 Evidence: low
Full summary, score breakdown and related studies → Original source
Despite differing white and grey matter retention characteristics, cortical retention for each (18)F tracer was highly correlated with that of PiB, enabling conversion of thresholds across tracer measurement scales with a high level of internal consistency. 2 key findings →
Participants: 40 Evidence: low
Full summary, score breakdown and related studies → Original source
Individuals with greater early- and middle-life cognitive activity had lower [(11)C]PiB uptake. 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →