These samples were graded on an ordinal scale and genotyped for variants associated with synucleinopathies. 2 key findings →
Participants: 213 Evidence: moderate
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.
Patients with the repeat expansion had significantly more co-morbid FTD than patients without the repeat (50%vs 12%), and a distinct pattern of non-motor cortex changes on high-resolution 3 T magnetic resonance structural neuroimaging. 3 key findings →
Design: longitudinal study Participants: 49 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Their results on motor testing from the preceding years were plotted, and then assessed with regression analysis, to determine when markers first deviated from normal values. 3 key findings →
Design: cohort study Participants: 78 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
From a total of 146 patients, 111 patients were included (67 men [60.4%]; mean [SD] age at diagnosis, 62.5 [11.5] years). 1 key finding →
Design: cohort study Participants: 146 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Mild cognitive impairment in Parkinson's disease is associated with progression to dementia (Parkinson's disease dementia) in a majority of patients. 5 key findings →
Design: longitudinal study Participants: 39 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The cumulative incidence of cognitive impairment was 8.5% at year 1, increasing to 47.4% by year 6. 2 key findings →
Design: prospective cohort Participants: 141 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
LATE-NC is a common TDP-43 proteinopathy, associated with an amnestic dementia syndrome that mimicked Alzheimer's-type dementia in retrospective autopsy studies. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
67/100
The Dementia with Lewy Bodies (DLB) Consortium has refined its recommendations about the clinical and pathologic diagnosis of DLB, updating the previous report, which has been in widespread use for the last decade. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Patients with FTLD were distributed between FTLD-tau (34 patients: 10 corticobasal degeneration, nine progressive supranuclear palsy, eight Pick's disease, three frontotemporal dementia with parkinsonism associated with chromosome 17, three unclassifiable tauopathy, and one argyrophilic grain disease); FTLD-TDP (55 patients: nine type A including one with motor neuron disease, 27 type B including 21 with motor neuron disease, eight type C with right temporal lobe presentations, and 11 unclassifiable including eight with motor neuron disease), FTLD-FUS (eight patients), and one patient with FTLD-ubiquitin proteasome system positive inclusions (FTLD-UPS) that stained negatively for tau, TDP-43, and FUS. 4 key findings →
Participants: 438 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
67/100
The evidence base for treating a range of nonmotor symptoms in PD has grown substantially in recent years. 2 key findings →
Participants: 37 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The heterogeneity of neurodegenerative diseases is a key confound to disease understanding and treatment development, as study cohorts typically include multiple phenotypes on distinct disease trajectories. 1 key finding →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
67/100
This study provides evidence for sex differences in the progression to cognitive impairment in PD, while specific cognitive features become more important indicators of progression with impending conversion to PDD. 3 key findings →
Design: longitudinal study Participants: 418 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
PD dementia (PDD) is associated with α-synuclein propagation, but coexistent Alzheimer's disease (AD) pathology may coexist. 4 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
High-level evidence related to pharmacological strategies for managing Lewy body dementia is rare. 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
A large proportion of the Medicare PD population resides in an LTCF. 2 key findings →
Design: cohort study Participants: 38,334 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
66/100
Although behavioral variant frontotemporal dementia (bvFTD) is classically defined by behavioral and socio-emotional changes, impairments often extend to other cognitive functions. 2 key findings →
Design: systematic review Participants: 181 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
REM sleep behaviour disorder (RBD) is a parasomnia characterized by the loss of normal skeletal muscle atonia during REM sleep with prominent motor activity accompanying dreaming. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
66/100
Frontotemporal lobar degeneration (FTLD) is the second most common cause of presenile dementia. 1 key finding →
Participants: 515 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In amyotrophic lateral sclerosis and neocortical Lewy body disease, co-pathologies associated with APOE ɛ4. 2 key findings →
Participants: 247 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
GBA mutations (β = 4.65; 95% CI, 1.72-7.58; P = .002), E326K (β = 3.42; 95% CI, 0.66-6.17; P = .02), and GBA variants combined as a single group (β = 4.01; 95% CI, 1.95-6.07; P = 1.5 × 10-4) were associated with a more rapid decline in MDS-UPDRS III score. 4 key findings →
Design: longitudinal study Participants: 740 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cognitive decline is a debilitating manifestation of disease progression in Parkinson's disease. 4 key findings →
Design: longitudinal study Participants: 3,200 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The impact of Parkinson's disease (PD) dementia is substantial and has major functional and socioeconomic consequences. 4 key findings →
Design: longitudinal study Participants: 486 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We concluded that cognitive training along with active tDCS is a useful combined approach in the management of mood and cognitive dysfunctions in PD. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The results suggest that standard and tailored cognitive training may improve executive function, attention/working memory, and memory in PD. 5 key findings →
Design: randomized controlled trial Evidence: high
Full summary, score breakdown and related studies → Original source
OH and RBD yielded individual and combined negative effects on disability in α-synucleinopathies, reflecting a 'malignant' phenotype of PD with early cognitive impairment and postural instability. 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 1,021 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Alpha-synuclein locus duplication as a cause of familial Parkinson's disease
- Elucidating the Role of Cerebellar Synaptic Dysfunction in C9orf72-ALS/FTD - a Systematic Review and Meta-Analysis
- The ALS/PDC syndrome of Guam and the cycad hypothesis
- MDS clinical diagnostic criteria for Parkinson's disease
- Neurofilament Light Chain and Differentiation of Behavioral Variant Frontotemporal Dementia From Psychiatric Disorders
- The Lewy body in Parkinson's disease: molecules implicated in the formation and degradation of alpha-synuclein aggregates
- MMSE and MoCA in Parkinson's disease and dementia with Lewy bodies: a multicenter 1-year follow-up study
- Clinical diagnosis of progressive supranuclear palsy: The movement disorder society criteria
- Neuroimaging and plasma biomarker differences and commonalities in Lewy body dementia subtypes
- Epilepsia como manifestación temprana en el espectro de la enfermedad de Alzheimer: explorando la variante epiléptica
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 →