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
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
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
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
At baseline, Aβ+ participants showed higher CP FWf, increased white matter hyperintensity (WMH) volume, and decreased diffusion tensor image analysis along the perivascular space (DTI-ALPS). 5 key findings →
Design: cohort study Participants: 216 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The gut-brain axis explains that changes in the intestinal microbiota influence Alzheimer's disease (AD). 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The microbiota-gut-brain axis (MGBA) is an intricate bidirectional communication network that links intestinal microbiota with the central nervous system (CNS) through immune, neural, endocrine, and metabolic pathways. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
= 0.009). Other neuropathologies were similar across cognitive groups. 4 key findings →
Design: cohort study Participants: 40 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Dementia is marked by progressive cognitive decline linked to oxidative stress, neuroinflammation, and synaptic dysfunction. 4 key findings →
Design: systematic review Participants: 29 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Aging and age-related diseases share convergent pathways at the proteome level. 1 key finding →
Participants: 43,616 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our results suggest that microstructural features derived from NODDI such as fISO might be useful adjunct markers to tau, which needs to be confirmed in longitudinal studies. 2 key findings →
Design: longitudinal study Participants: 80 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Individuals with Down syndrome (DS) have a genetically determined form of Alzheimer's disease (AD) due to the amyloid precursor protein (APP) gene dose effect. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We identified 59 key microbial species linked to MCI and AD biomarkers. 5 key findings →
Participants: 119 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Amyloid burden impacts cognitive decline in the pre-dementia stages of Alzheimer's disease (AD), but there remains significant variability in cognitive trajectories that may be explainable by markers of synaptic function and neurodegeneration. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This systematic review aims to elucidate the neuropathological basis of the HIDA and psychosis domains, exploring whether distinct proteinopathies and neural circuit dysfunctions are associated with these symptoms. 4 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Clinical Dementia Rating-Global scores (1.44 ± 0.65 versus 0.24 ± 0.25; P < 0.0001) and Patient Health Questionnaire-9 scores (4.88 ± 4.21 versus 0.20 ± 0.50; P < 0.0001) were higher than controls. 4 key findings →
Design: cross-sectional Participants: 25 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Primary age-related tauopathy (PART) was proposed in 2014 as a neuropathological term to describe patients with Alzheimer's-type medial temporal lobe neurofibrillary degeneration in the absence of significant β-amyloid pathology. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
= 0.038) over time. Physical activity was associated with less synaptic dysfunction and cognitive activity with less synaptic dysfunction and lower amyloid burden over time, albeit effect sizes were small. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Nutritional supplementation is emerging as a promising strategy to support clinical management of early Alzheimer's disease (AD), partly through modulation of the intestinal microbiome via the microbiota-gut-brain axis. 1 key finding →
Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source
They remain a significant focus of scientific and clinical interest due to their increasing medical and social importance. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Synaptic degeneration has been linked to cognitive decline. 5 key findings →
Participants: 187 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma pTau217 levels serve as a scalable, non-invasive marker of AD-pathology across Lewy body diseases, PSP/CBS, and MCI/CU populations. 2 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
-heterozygous human brain tissue was reactivated in response to neuroinflammation caused by exposure to other pathogens. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer's disease (AD) represents the most prevalent neurodegenerative disorder and leading cause of dementia worldwide, with its incidence rising dramatically in aging populations. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Menopause is a major biological transition that may influence women's late-life brain health. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Synucleinopathies, such as Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy, are characterized by the aggregation of α-synuclein. 1 key finding →
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 (3.7% 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 →