43/100
Here, we show that cofilin is hyper-phosphorylated in human ALS and disease models compared to controls. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Mutations in the ANXA11 gene, encoding an RNA-binding protein, have been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS), but the underlying in vivo mechanisms remain unclear. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We identified 34 epidemiological studies that met the inclusion criteria. 5 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Copy number variation (CNV) of the amyloid-β precursor protein gene (APP) is a known cause of autosomal dominant Alzheimer disease (ADAD), but de novo genetic variants causing ADAD are rare. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent reports suggest dysregulation of the N6-methyladenosine (m6A) RNA modification may contribute to the pathology of neurodegenerative diseases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The concomitant depletion of dopaminergic and serotonergic inputs within the hippocampus of C57BL/6N mice provokes a pronounced activation of microglia via the NLRP3-inflammasome pathway, accompanied by increased IL-1β expression. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Mitochondrial oxidative stress and neuroinflammation are involved in the onset and progression of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Vascular cognitive impairment and dementia (VCID) is increasingly recognized as one of the leading causes of cognitive decline in aging populations. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) represents the most common cause of dementia and urgently requires sensitive biomarkers and effective therapies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
43/100
In PD patients, a decrease in [ 18 F]DOPA PET retention correlated with disease duration as well as CSF neurodegenerative and synaptic biomarkers but not with inflammatory biomarkers or [ 18 F]RO948 PET midbrain off-target retention. 2 key findings →
Participants: 623 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Tauopathies are neurodegenerative diseases characterized by pathological tau protein inclusions and dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Metabolic syndrome markers, such as insulin resistance and the triglyceride/HDL C ratio, correlate with early cognitive impairment. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
43/100
α -Syn positivity was detected in 9% of CU individuals, a lower rate than in clinically impaired participants with AD (16%) and LBD diagnoses (81%). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
43/100
This method differentiated eight tauopathies, including Alzheimer's disease, Pick disease, progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), argyrophilic grain disease (AGD), frontotemporal dementia with parkinsonism associated with chromosome 17 with N279K mutation (FTDP-17 N279K), and globular glial tauopathies types II and III. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our findings revealed significantly elevated CSF GAP-43 levels in individuals with AD compared to CN and MCI groups. 4 key findings →
Participants: 1,639 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by memory loss and cognitive decline, with women being disproportionately affected in both prevalence and severity. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
LLMD participants were more likely to be tau PET and Aβ PET positive than HCs. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
At baseline, MCI participants displayed elevated levels of IL-17A, CX3CL1, CCL11, with a borderline increase of IL-6 and TNFα. 5 key findings →
Participants: 76 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
To date, the impact of cognitive therapies on patients with dementia and mild cognitive impairment (MCI) has been studied in terms of cognition, quality of life and activities of daily living rather than in the context of neuropsychiatric symptoms (NPS). 5 key findings →
Participants: 4,089 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our study shows that the pdp is well received by its participants, underlined by a high level of satisfaction and positive responses to what pdp offers. 5 key findings →
Participants: 575 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The Hierarchical-Circular Model of Biological Memory offers a unifying hypothesis for Alzheimer's disease and related dementias that bridges genetic, epigenetic, physiological, neuroimmune, and interoceptive processes across the lifespan. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Participants numbered 3334 and had a median age of 62 years. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Data on 214 251 respondents were included in the study. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
43/100
Dementia, a syndrome characterized by a decline in cognitive function beyond what is expected from normal aging, poses a significant global health challenge. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Higher general burden was associated with female caregivers (β = −.19, p = .05), higher education (β = .16, p = .03), caring for someone with dementia (β = .36, p = .01), and greater dysphagia-related burden (β = .33, p = .01). 5 key findings →
Participants: 211 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Where “Free full text” comes from
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.
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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.
What this library is — and isn't
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 →