27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Patients with AD spectrum demonstrated altered GM abundance, which was differentially mediated by countries and clinical stages. 5 key findings →
Design: systematic review Participants: 427 Evidence: high
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is projected to become the highest-burden neurological disorder globally. 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease (AD), tau undergoes abnormal post-translational modifications and aggregations. 5 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
At randomization, the mean age is 72, 50% female, 77% with CDR-global score 0.5, and mean MMSE score 23.8. 5 key findings →
Design: clinical trial Participants: 464 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Limbic-predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) and Alzheimer's disease neuropathologic change (ADNC) are each associated with substantial cognitive impairment in aging populations. 2 key findings →
Design: longitudinal study Participants: 5,665 Evidence: moderate
Full summary, score breakdown and related studies → Original source
SNAP-25 and 14-3-3 zeta/delta also had the strongest associations with tau-PET, amyloid-β-PET and cortical thickness at baseline and were associated with longitudinal changes in these imaging biomarkers [β(standard error, SE) = -0.056(0.0006) to 0.058(0.005), P < 0.0001]. 3 key findings →
Design: longitudinal study Participants: 205 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Probiotic supplements were shown to improve cognitive function in Alzheimer's disease (AD) patients. 2 key findings →
Participants: 21 Evidence: low
Full summary, score breakdown and related studies → Original source
The evolution of the understanding of the intestinal microbiota and its influence on our organism leverages it as a potential protagonist in therapies aimed at diseases that affect not only the intestine but also neural pathways and the central nervous system itself. 5 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
This population-based cohort study demonstrates significant association between IBD and subsequent development of dementia. 5 key findings →
Design: cohort study Participants: 1,742 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cognitive frailty, defined as the coexistence of mild cognitive impairment symptoms and physical frailty phenotype in older persons, is increasingly considered the main geriatric condition predisposing to dementia. 4 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Serum IgG levels to common periodontal microbiota are associated with risk for developing incident AD. 5 key findings →
Design: cohort study Participants: 219 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Insoluble tau aggregates within neurofibrillary tangles are a defining neuropathological feature of Alzheimer’s disease (AD) and closely correlate with clinical symptoms. 2 key findings →
Participants: 108 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The chronological progression of brain atrophy over decades, from pre-symptomatic to dementia stages, has never been formally depicted in Alzheimer's disease. 2 key findings →
Design: cross-sectional Participants: 3,512 Evidence: moderate
Full summary, score breakdown and related studies → Original source
CSF-soluble misfolded α-synuclein aggregates (seeds) are readily detected in people with Parkinson's disease by α-synuclein seed amplification assay (synSAA), but identification of seeds associated with multiple system atrophy for diagnostic purposes has proven elusive. 2 key findings →
Design: cohort study Participants: 80 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Tau is common in LBD and may reduce clinical diagnostic accuracy in people with DLB. 2 key findings →
Design: meta-analysis Participants: 1,511 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The maximal tolerated dose of PQ912 has been identified and the results support future studies at still lower doses reaching > 50% target occupancy, a longer up-titration phase to potentially induce adaptation and longer treatment periods to confirm the early signals of efficacy as seen in this study. 4 key findings →
Design: randomized controlled trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Emerging evidence suggests a potential role of gut dysbiosis in neurodegenerative disorders and, in particular, Alzheimer's disease (AD) pathology and cognitive decline. 4 key findings →
Design: cross-sectional Participants: 49 Evidence: moderate
Full summary, score breakdown and related studies → Original source
It has been more than 10 years since it was first proposed that the neurodegeneration in Alzheimer's disease (AD) may be caused by deposition of amyloid beta-peptide (Abeta) in plaques in brain tissue. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Cerebral deposition of amyloid beta peptide (Abeta) is an early and critical feature of Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disorder characterized pathologically by ubiquitinated TAR DNA binding protein (TDP-43) inclusions. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In particular, systemic inflammation, vascular inflammation, and altered endothelial function may play roles in domain-specific cognitive decline of nondemented individuals. 1 key finding →
Design: randomized controlled trial Participants: 1,159 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study analyzed 80,660 single-nucleus transcriptomes from the prefrontal cortex of 48 individuals with varying degrees of Alzheimer's disease pathology to examine molecular and cellular changes across six major brain cell types. 4 key findings →
Full summary, score breakdown and related studies → Original source Free full text
Hypersynchronization has been proposed as a synaptic dysfunction biomarker in the Alzheimer's disease continuum, reflecting the alteration of the excitation/inhibition balance. 5 key findings →
Design: longitudinal study Participants: 27 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive, degenerative disorder of the central nervous system. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau hyperphosphorylation is an early step in tau-mediated neurodegeneration and is associated with intracellular aggregation of tau as neurofibrillary tangles, neuronal and synaptic loss, and eventual cognitive dysfunction in Alzheimer disease. 3 key findings →
Design: randomized controlled trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →