In APPL/S mice, BD10-2 treatment improved memory and LTP deficits. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Immunotherapies targeting extracellular tau share the premise that interrupting cell-to-cell spread of tau pathology in Alzheimer's disease (AD) will slow dementia pathogenesis. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the present study, we found senescent aVICs exhibited impaired macroautophagy/autophagy as evidenced by compromised autophagy flux and immature autophagosomes. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
46/100
Here, we integrated multiple approaches to characterize proteasome function, composition and regulation in post-mortem human AD brain tissue compared with age-matched controls. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aging leads to progressive decline in organ and tissue integrity and function, partly due to loss of proteostasis and autophagy malfunctioning. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Among the natural extracts tested, PanQ emerged as the most effective for increasing the active CatB isoform in correspondence with enhanced levels of synaptic proteins and the autophagy marker LC3-II. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurons with lower basal UPS activity were more vulnerable to tau accumulation following mild UPS inhibition. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The autophagy-lysosome pathway (ALP) and the ubiquitin-proteasome system (UPS) are the primary protein degradative mechanisms maintaining proteostasis in neurons. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Diabetic retinopathy (DR) and Alzheimer's disease (AD) are progressive neurodegenerative disorders affecting the eye and the brain, respectively. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The 4R-like pattern was more prevalent and more strongly expressed (84.3%, mean score, 2.0 ± 1.1) in patients with a consensus diagnosis of PSP/CBD (joint diagnostic group of clinically likely 4R tauopathies) than in all other groups (11.6%, 0.26 ± 0.75, P < 0.0001). 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The study population demonstrated limited PET-based amyloid-β and tau pathology, which did not associate with any of the investigated plasma biomarkers. 5 key findings →
Design: cross-sectional Participants: 49 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Using the RGC marker ribonucleic acid binding protein with multiple splicing (RBPMS) and Nissl staining, we found a 46–56% reduction in RBPMS + RGCs and Nissl + neurons in the ganglion cell layer (GCL) of MCI and AD retinas ( P < 0.05–0.001). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD), the most common cause of dementia, is characterized by the accumulation of amyloid-β (Aβ) in senile plaques and abnormally hyperphosphorylated tau proteins in neurofibrillary tangles. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
CSF and plasma SNAP25 were positively correlated, but no correlation was observed for VAMP2 in these matrices. 5 key findings →
Participants: 80 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Aggregation of microtubule-associated tau protein is a distinct hallmark of several neurodegenerative disorders such as Alzheimer’s disease (AD), dementia with Lewy bodies (DLB), and progressive supranuclear palsy (PSP). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neurodegenerative diseases are characterized by protein aggregation and overlapping pathologies, challenging traditional classifications and highlighting shared underlying mechanisms. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease is a neurodegenerative disorder characterized by two hallmarks: amyloid beta plaques and neurofibrillary tangles. 2 key findings →
Participants: 708,580 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mutations in the presenilin genes are the main cause of familial Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the healthy adult brain synapses are continuously remodelled through a process of elimination and formation known as structural plasticity. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
See Attems and Jellinger (doi:10.1093/brain/awx360) for a scientific commentary on this article. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a heterogeneous disorder with multiple etiologies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Familial forms of frontotemporal dementia (FTD) with tauopathy are mostly caused by mutations in the gene encoding the microtubule-associated protein tau (MAPT). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tauopathies are a diverse group of progressive and fatal neurodegenerative diseases characterized by aberrant tau inclusions in the central nervous system. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although multiple CHCHD10 mutations are associated with the spectrum of familial and sporadic frontotemporal dementia-amyotrophic lateral sclerosis (FTD-ALS) diseases, neither the normal function of endogenous CHCHD10 nor its role in the pathological milieu (that is, TDP-43 pathology) of FTD/ALS have been investigated. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recently intronic and exonic mutations in the Tau gene have been found to be associated with familial neurodegenerative syndromes characterized not only by a predominantly frontotemporal dementia but also by the presence of neurological signs consistent with the dysfunction of multiple subcortical neuronal circuitries. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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. Show only studies that are free to read
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 →