Diabetes is a significant modifiable risk factor for cognitive dysfunction. 1 key finding →
Design: open-label trial Participants: 396 Evidence: high
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.
Gantenerumab reduced amyloid PET load, CSF biomarkers of amyloid beta (Aβ)40, total tau (t-tau), phosphorylated tau 181 (p-tau181), neurogranin, S100 calcium-binding protein B (S100B), neurofilament light (NfL), alpha-synuclein (α-syn), neuronal pentraxin-2 (NPTX2), and plasma biomarkers of t-tau, p-tau181, p-tau217, and glial fibrillary acidic protein (GFAP) while increasing plasma Aβ40, Aβ42. vMRI showed increased reduction in whole brain volume and increased ventricular expansion, while hippocampal volume was unaffected. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Repurposed drugs provide a rich source of potential therapies for Alzheimer's disease (AD) and other neurodegenerative disorders (NDD). 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Parkinson's disease (PD) research is beginning to focus on early disease modification and prevention. 2 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
45/100
Cholinesterase inhibitors with additional nicotinic activity, such as galantamine, may be useful in PD patients with dementia (PDD) since stimulation of nicotinic receptors may prevent the down-regulation that is likely to accompany cholinesterase inhibition and facilitate dopamine release in the striatum. 4 key findings →
Design: open-label trial Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Drug development continues robustly at all phases despite setbacks in several programs in the recent past. 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
The plasma p-tau217 and plasma GFAP models adequately predicted the change over time, with donanemab resulting in decreased plasma p-tau217 and plasma GFAP concentrations. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
The intersection of metabolic disease and neurodegeneration represents one of the most consequential frontiers in translational neuroscience. 3 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
GBA-related PD (GBA-PD) patients have higher risk of dementia and reduced survival than non-carriers. 3 key findings →
Design: open-label trial Evidence: low
Full summary, score breakdown and related studies → Original source
Drug development for Alzheimer disease and other neurodegenerative dementias, including frontotemporal dementia, has experienced a long history of phase 2 and phase 3 clinical trials that failed to show efficacy of investigational drugs. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Regions were heterogeneous at baseline. At baseline, disease severity as measured by ADAS-cog11, ADCS-ADL, and CDR-SB was numerically worse for Eastern Europe/Russia compared with other regions. 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source
The Alzheimer disease (AD) neuropathological hallmarks amyloid β (Aβ) and tau neurofibrillary (NF) pathology have been reported in the olfactory bulb (OB) in aging and in different neurodegenerative diseases, which coincides with frequently reported olfactory dysfunction in these conditions. 1 key finding →
Design: clinical trial Evidence: moderate
Full summary, score breakdown and related studies → Original source
BBBO was achieved in 5 out of 6 subjects with an average volume of 983±626 mm 3 following FUS at the right frontal lobe both in white and gray matter regions. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
44/100
Alzheimer disease (AD) is a chronic neurodegenerative disorder with complex pathophysiology that affects over 50 million people worldwide. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Many trials of drugs aimed at preventing or clearing β-amyloid pathology have failed to demonstrate efficacy in recent years and further trials continue with drugs aimed at the same targets and mechanisms. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Individuals with Down syndrome (DS) develop Alzheimer's disease (AD)-related neuropathology, characterized by amyloid plaques with amyloid β (Aβ) and neurofibrillary tangles with tau accumulation. 3 key findings →
Design: clinical trial Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
All patients taking donepezil completed the 30 days of treatment without adverse effects. 3 key findings →
Design: clinical trial Participants: 30 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Galantamine appears to be an effective and safe therapy for patients with DLB. 2 key findings →
Design: open-label trial Participants: 50 Evidence: low
Full summary, score breakdown and related studies → Original source
Key results included a 35% slowing of decline on the Integrated Alzheimer's Disease Rating Scale (iADRS) and a 36% slowing on the Clinical Dementia Rating-Sum of Boxes (CDR-SB). 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Twelve cases of dementia were diagnosed among individuals with scores below cutoff point and one among subjects with high scores. 2 key findings →
Design: clinical trial Participants: 1,611 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Previous data from familial AD due to mutations in presenilin 1 and presenilin 2 genes and the amyloid precursor protein suggest that the long form of Abeta peptide, Abeta42, is selectively increased in these circumstances. 3 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
MCI represents a prodromal stage of AD, and inflammation occurs as one of the earliest pathological events in AD. 5 key findings →
Design: clinical trial Participants: 62 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The pathogenesis of HIV-associated cognitive changes is poorly understood. 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Administration of hUCB-MSCs into the hippocampus and precuneus by stereotactic injection was feasible, safe, and well tolerated. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Aducanumab is a monoclonal antibody selective for amyloid β (Aβ) aggregates. 2 key findings →
Design: clinical trial 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 →