Parkinson's disease dementia (PDD) is associated with cholinergic deficits. 4 key findings →
Participants: 550 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Parkinson's disease dementia (PDD) is associated with cholinergic deficits. 4 key findings →
Participants: 550 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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
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
Although dopamine replacement therapy remains a core component of Parkinson's disease treatment, the onset of motor fluctuations and dyskinetic movements might require a range of medical and surgical approaches from a multidisciplinary team, and important new approaches in the delivery of dopamine replacement are becoming available. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Patients with Parkinson's disease have a number of specific visual disturbances. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The Lewy body is a distinctive neuronal inclusion that is always found in the substantia nigra and other specific brain regions in Parkinson's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The micro-architecture of the substantia nigra was studied in control cases of varying age and patients with parkinsonism. 2 key findings →
Evidence: low
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Progressive supranuclear palsy (PSP) is a clinical syndrome comprising supranuclear palsy, postural instability, and mild dementia. 1 key finding →
Evidence: low
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Dementia is common in Parkinson's disease (PD) but measures that track cognitive change in PD are lacking. 4 key findings →
Participants: 100 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Earlier AutD is associated with a more rapid development of disease milestones and shorter survival in patients with PD. 5 key findings →
Participants: 100 Evidence: low
Full summary, score breakdown and related studies → Original source
The clinical syndrome of pure akinesia has most often been associated with progressive supranuclear palsy (PSP) and is characterized by difficulty initiating gait and "freezing" during walking, writing and speaking. 1 key finding →
Participants: 749 Evidence: low
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The authors studied the accuracy of clinical diagnosis of idiopathic PD (IPD) in 100 consecutive clinically diagnosed cases that came to neuropathological examination. 1 key finding →
Evidence: low
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To investigate the relationships between age, the advanced clinical stages of Parkinson's disease and neuropathology, we surveyed 129 case records from donors with pathologically proven Parkinson's disease at the Queen Square Brain Bank for Neurological Disorders. 4 key findings →
Evidence: low
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Amyloid-beta (Abeta) peptide pathology in Alzheimer's disease (AD) comprises extracellular plaques and cerebral amyloid angiopathy (CAA). 1 key finding →
Evidence: low
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The degeneration of neurones in Parkinson's disease (PD) may involve oxidative stress. 2 key findings →
Evidence: low
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The clinical details of 100 cases of histologically confirmed Parkinson's disease were examined and correlated with pathologic findings. 5 key findings →
Evidence: low
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Progressive supranuclear palsy-parkinsonism (PSP-P) is a primary tauopathy characterised by neurofibrillary degeneration, which is frequently mistaken for Parkinson's disease (PD), multiple system atrophy (MSA), and vascular parkinsonism (VP) at presentation. 5 key findings →
Participants: 444 Evidence: low
Full summary, score breakdown and related studies → Original source
The pathological findings of corticobasal degeneration are associated with several distinct clinical syndromes, and the corticobasal syndrome has been linked with a number of diverse pathologies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Groups of patients with idiopathic Parkinson's disease, multiple system atrophy, and progressive supranuclear palsy or Steele-Richardson-Olszewski syndrome, matched for overall clinical disability, were compared using three computerised cognitive tests previously shown to be sensitive to frontal lobe dysfunction. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Measures to prevent the morbidity associated with falls and fractures in bradykinetic rigid syndromes may be best directed at patients with the risk factors identified in this study. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In comparison with other Parkinsonian syndromes the patients were older and had an extremely low frequency of visual hallucinations compared with Parkinson's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
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.
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.
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 →