31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The accumulation of pathological misfolded tau is a feature common to a collective of neurodegenerative disorders known as tauopathies, of which Alzheimer's disease (AD) is the most common. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tauopathies are neurodegenerative diseases characterized by aberrant forms of tau protein accumulation leading to neuronal death in focal brain areas. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Determining the relative contribution of amyloid plaques and neurofibrillary tangles to brain dysfunction in Alzheimer disease is critical for therapeutic approaches, but until recently could only be assessed at autopsy. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Extracellular deposition of amyloid-β as neuritic plaques and intracellular accumulation of hyperphosphorylated, aggregated tau as neurofibrillary tangles are two of the characteristic hallmarks of Alzheimer's disease 1,2 . 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The geometric distribution and increased burden of retinal amyloid pathology in AD, together with the feasibility to noninvasively detect discrete retinal amyloid deposits in living patients, may lead to a practical approach for large-scale AD diagnosis and monitoring. 5 key findings →
Participants: 37 Evidence: low
Full summary, score breakdown and related studies → Original source
Most participants were cognitively normal (427 of 491 [87%]) and the mean age was 69.0 ± 8.8 years. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is associated with inner retina (nerve fiber and ganglion cell layers) thinning. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
The single nucleotide polymorphism (SNP) rs744373 in the bridging integrator-1 gene (BIN1) is a risk factor for Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The abnormal accumulation of amyloid-β and tau targets specific spatial networks in Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In this study, we aimed to assess whether women are able to withstand more tau before exhibiting verbal memory impairment. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings suggest that CSF pTau/Aβ 40 may be a superior measure of tauopathy compared to CSF pTau alone, and CSF pTau/Aβ 40 enables detection of tau accumulation at an earlier stage than FTP among Aβ+ individuals. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Molecular PET shows expected correlations with Alzheimer-related pathology but lacks sensitivity to detect mild Alzheimer pathology in FTLD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Network characteristics in women may favor an accelerated brain-wide tau spread leading to a higher tau burden in women than men with MCI with implications for the greater female preponderance in Alzheimer's disease diagnosis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglial activation was elevated in dementia with Lewy bodies subjects with mild disease when compared to those with moderate/severe impairment, where disease severity was indexed by cognitive performance on the revised Addenbrooke's Cognitive Examination. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Pattern of diffusion tensor MRI (DTI) alterations were investigated in pathologically-staged Alzheimer's disease (AD) patients (n = 46). 4 key findings →
Participants: 46 Evidence: low
Full summary, score breakdown and related studies → Original source
We describe two patients with mitochondrial myopathies who presented with complex multisystem diseases predominantly affecting the central nervous system. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We describe a family with nearly 300 members over 8 generations with 32 affected individuals who have an autosomal dominant neurodegenerative disease characterized by progressive parkinsonism with dystonia unrelated to medications, dementia, ocular motility abnormalities, pyramidal tract dysfunction, frontal lobe release signs, perseverative vocalizations, and urinary incontinence. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We report the neuropathological evaluation of a 24-year-old autistic woman suffering from a residual state of infantile autism and presenting with self-injury behavior since childhood. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The segmentation application revealed ganglion cell and retinal layer atrophy in patients with AD compared with controls, especially in the inner layers of patients with long disease duration. 3 key findings →
Participants: 150 Evidence: low
Full summary, score breakdown and related studies → Original source
The aggregation of amyloid-beta peptide and tau protein dysregulation are implicated to play key roles in Alzheimer's disease pathogenesis and are considered the main pathological hallmarks of this devastating disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
High dietary cholesterol and low dietary docosahexaenoic acid (DHA) intake are risk factors for Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease and its clinical variants have characteristic spatial and temporal progression patterns of amyloid and tau driving symptomatology, but the distribution of microglia density, as measured by 18kDa translocator protein (TSPO) PET, is unknown. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In vivo imaging of fibrillar β-amyloid deposits may assist clinical diagnosis of Alzheimer's disease (AD), aid treatment selection for patients, assist clinical trials of therapeutic drugs through subject selection, and be used as an outcome measure. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer disease (AD) is associated with the accumulation in the brain of extracellular neuritic plaques composed mainly of β-amyloid (Aβ) and of intracellular neurofibrillary tangles composed of hyperphosphorylated forms of the microtubule-associated protein tau. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The human brain contains about 100 billion neurons forming an intricate network of innumerable connections, which continuously adapt and rewire themselves following inputs from external and internal environments as well as the physiological synaptic, dendritic and axonal sculpture during brain maturation and throughout the life span. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.
1,048 records (3.3% of the library) are not peer-reviewed — 973 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events