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In a medical emergency, call 911. More numbers, and what each line does, on the help page.

Find studies

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

Frontotemporal dementia and its subtypes: a genome-wide association study

✓ Peer-reviewed alzhub usefulness score 78 out of 100. The Lancet. Neurology 2014-07-01

Frontotemporal dementia (FTD) is a complex disorder characterised by a broad range of clinical manifestations, differential pathological signatures, and genetic variability. 4 key findings →

Design: meta-analysis Participants: 3,526 Evidence: high

Substantial variation in the prevalence of dementia in Parkinson's disease (PDD) has been reported. 2 key findings →

Design: systematic review Participants: 1,767 Evidence: high

Outpatient PC is associated with benefits among patients with PDRD compared with standard care alone. 5 key findings →

Participants: 584 Evidence: high

Dementia has been increasingly more recognized to be a common feature in patients with Parkinson's disease (PD), especially in old age. 4 key findings →

Design: systematic review Evidence: high

Frontotemporal lobar degeneration with neuronal inclusions of the TAR DNA-binding protein 43 (FTLD-TDP) is a fatal neurodegenerative disorder with only a limited number of risk loci identified. 3 key findings →

Design: meta-analysis Participants: 985 Evidence: high

We tested the hypothesis that plasma neurofilament light chain (NfL) identifies asymptomatic carriers of familial frontotemporal lobar degeneration (FTLD)-causing mutations at risk of disease progression. 4 key findings →

Design: longitudinal study Participants: 277 Evidence: moderate

A mean value of 85.7% was achieved for overall diagnostic accuracy, 82.4% for positive predictive value, and 87.5% for negative predictive value. 2 key findings →

Participants: 94 Evidence: low

Parkinson risk in idiopathic REM sleep behavior disorder: preparing for neuroprotective trials

✓ Peer-reviewed alzhub usefulness score 71 out of 100. Neurology 2015-02-13

Using stratification with simply assessed markers, it is now not only possible, but practical to include patients with RBD in neuroprotective trials against Parkinson disease, multiple system atrophy, and dementia with Lewy bodies. 3 key findings →

Design: prospective cohort Participants: 89 Evidence: moderate

As none of the studies exceeded a duration of 6 months, the recommendations given are for the short-term management of the different non-motor symptoms. 5 key findings →

Design: randomized controlled trial Evidence: high

At 6 months, compared with usual care, participants receiving the intervention had better QOL (QOL-AD score, 0.09 [95% CI, -0.63 to 0.82] vs -0.88 [95% CI, -1.62 to -0.13]; treatment effect estimate, 0.97; 95% CI, 0.07-1.86; P = .03). 4 key findings →

Participants: 612 Evidence: high

We have demonstrated that three baseline measures, namely, age >or=72 years, semantic fluency less than 20 words in 90 s and inability to copy an intersecting pentagons figure, are significant predictors of dementia risk, thus validating our previous findings. 5 key findings →

Design: cross-sectional Participants: 126 Evidence: moderate

Neuropathology underlying clinical variability in patients with synucleinopathies

✓ Peer-reviewed alzhub usefulness score 70 out of 100. Acta neuropathologica 2011-07-01

Abnormal aggregates of the synaptic protein, α-synuclein, are the dominant pathology in syndromes known as the synucleinopathies. 1 key finding →

Design: meta-analysis Evidence: high

Common genetic variance in apolipoprotein E (APOE), β-glucocerebrosidase (GBA), microtubule-associated protein tau (MAPT), and α-synuclein (SNCA) has been linked to cognitive decline in Parkinson's disease (PD), although studies have yielded mixed results. 4 key findings →

Design: longitudinal study Participants: 281 Evidence: moderate

Identifying concomitant Lewy body (LB) pathology through seed amplification assays (SAA) might enhance the diagnostic and prognostic work-up of Alzheimer's disease (AD) in clinical practice and trials. 2 key findings →

Design: cohort Participants: 795 Evidence: moderate

Diagnosis Across the Spectrum of Progressive Supranuclear Palsy and Corticobasal Syndrome

✓ Peer-reviewed alzhub usefulness score 69 out of 100. JAMA neurology 2020-03-01

Patients in the CBS-AD group had a longer diagnostic latency, relatively benign clinical trajectory, greater cognitive impairment, and higher APOE-ε4 allele frequency than those in the CBS-non-AD group (AUC, 0.80-0.87; P Conclusions and relevance These findings suggest that studies focusing on the PSP-RS subtype are likely to miss a large number of patients with underlying PSP tau pathology. 2 key findings →

Design: cohort study Participants: 76 Evidence: moderate

A clinico-pathological study of subtypes in Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 69 out of 100. Brain : a journal of neurology 2009-09-16

We have carried out a systematic review of the case files of 242 donors with pathologically verified Parkinson's disease at the Queen Square Brain Bank for Neurological Disorders in an attempt to corroborate the data-driven subtype classification proposed by Lewis and colleagues (Heterogeneity of Parkinson's disease in the early clinical stages using a data driven approach. 4 key findings →

Design: systematic review Evidence: high

Association of Antipsychotic Use With Mortality Risk in Patients With Parkinson Disease

✓ Peer-reviewed alzhub usefulness score 69 out of 100. JAMA neurology 2016-05-01

The use of APs by patients with dementia in the general population is associated with increased mortality, but whether this risk extends to patients with PD remains unknown. 5 key findings →

Design: cohort study Participants: 7,877 Evidence: moderate

Evolution of cognitive dysfunction in an incident Parkinson's disease cohort

✓ Peer-reviewed alzhub usefulness score 68 out of 100. Brain : a journal of neurology 2007-05-29

We have previously performed detailed clinical and neuropsychological assessments in a community-based cohort of patients with newly diagnosed parkinsonism, and through analysis of a subcohort with idiopathic Parkinson's disease (PD), we have demonstrated that cognitive dysfunction occurs even at the time of PD diagnosis and is heterogeneous. 1 key finding →

Design: longitudinal study Participants: 126 Evidence: moderate

In multivariate analyses, baseline age, University of Pennsylvania Smell Inventory Test (UPSIT) scores, CSF amyloid - (Aβ 42 ) to t-tau ratio, and APOE status were associated with change in MoCA scores over time. 5 key findings →

Design: cohort study Participants: 390 Evidence: moderate

Prevalence and characteristics of dementia in Parkinson disease: an 8-year prospective study

✓ Peer-reviewed alzhub usefulness score 68 out of 100. Archives of neurology 2003-03-01

More than three quarters of this representative PD cohort developed dementia during the 8-year study period. 2 key findings →

Design: longitudinal study Participants: 224 Evidence: moderate

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.

↑ Change the filters

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 →

Newest studies, as a dated timeline →    Atom feed