30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
PET imaging with (11)C-labeled Pittsburgh Compound-B ((11)C-PIB) helps discriminate Alzheimer disease (AD) from frontotemporal lobar degeneration (FTLD). 2 key findings →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source
This study suggests that amyloid load is significantly raised in over 80% of subjects with DLB, while amyloid pathology is infrequent in PDD. 5 key findings →
Participants: 13 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Activation of microglia by classical inflammatory mediators can convert astrocytes into a neurotoxic A1 phenotype in a variety of neurological diseases 1,2 . 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Multiple avenues of research including epidemiology, molecular genetics and cell biology have identified links between Parkinson's disease and type 2 diabetes mellitus. 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source
Despite an ever-growing prevalence and increasing economic burden of Alzheimer's disease (AD) and Parkinson's disease (PD), recent advances in drug development have only resulted in minimally effective treatment. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
With decreasing local and global connectivity parameters, the large-scale functional brain network organization in AD deviates from the optimal 'small-world' network structure towards a more 'random' type. 5 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source
Confrontation naming is impaired in neurodegenerative conditions like Alzheimer's disease (AD), frontotemporal dementia (FTD) and corticobasal degeneration (CBD). 3 key findings →
Participants: 50 Evidence: low
Full summary, score breakdown and related studies → Original source
We studied 30 necropsy cases of vascular dementia with a lacunar state. 5 key findings →
Participants: 30 Evidence: low
Full summary, score breakdown and related studies → Original source
Under normal conditions, vivid dream mentation combined with skeletal muscle paralysis characterizes rapid eye movement sleep. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Neuropathologic etiologies of PPCD were Alzheimer disease (AD) (n = 13), AD plus Parkinson disease (n = 1), AD-Lewy body variant (n = 2), dementia with Lewy bodies plus progressive subcortical gliosis of Neumann (n = 1), corticobasal degeneration (n = 2), and prion-associated diseases: Creutzfeldt-Jakob disease (n = 1) and fatal familial insomnia (n = 1). 3 key findings →
Participants: 13 Evidence: low
Full summary, score breakdown and related studies → Original source
Missense mutations in the alpha-synuclein gene cause familial Parkinson's disease (PD), and alpha-synuclein is a major component of Lewy bodies (LBs) in sporadic PD, dementia with LBs (DLB), and the LB variant of Alzheimer's disease (AD). 3 key findings →
Participants: 65 Evidence: low
Full summary, score breakdown and related studies → Original source
(1) The overall sensitivity of the NINCDS-ADRDA criteria in diagnosing "probable" AD from 56 patients with cortical dementia (AD and FTD) was 0.93. 5 key findings →
Participants: 56 Evidence: low
Full summary, score breakdown and related studies → Original source
These results indicate that FS (p-tau231 and MMSE) has a strong potential to provide an early distinction between AD and VaD. 4 key findings →
Participants: 198 Evidence: low
Full summary, score breakdown and related studies → Original source
Moreover, our results revealed associations between NfL and disease severity in FTD and between tauopathy and episodic memory and lexical-semantic impairment in prodromal-AD. 5 key findings →
Participants: 72 Evidence: low
Full summary, score breakdown and related studies → Original source
Our results with asymmetrical presentations extend current knowledge about this rare AD variant. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amygdala, hippocampus and six cortical gyri were examined for the Lewy body (LB) degeneration and Alzheimer's disease (AD) type changes in 45 patients with Parkinson's disease (PD). 5 key findings →
Participants: 45 Evidence: low
Full summary, score breakdown and related studies → Original source
VGF levels are consistently decreased in brain tissue and CSF samples from patients with Alzheimer's disease compared to controls, and its levels correlate with disease severity and Alzheimer's disease pathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The FTP standardized uptake value ratios (inferior cerebellar gray reference region) and W-score (age-adjusted z-score) maps were compared with phosphorylated tau immunohistochemical analysis with monoclonal antibody CP13. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our study found that CIS on FDG-PET is not associated with fibrillar β-amyloid deposition but indicates lower Braak NFT stage in patients with DLB. 2 key findings →
Participants: 39 Evidence: low
Full summary, score breakdown and related studies → Original source
Extensive changes in resting-state oscillatory brain activity have recently been demonstrated using magnetoencephalography (MEG) in moderately advanced, non-demented Parkinson's disease patients relative to age-matched controls. 5 key findings →
Participants: 37 Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal lobar degeneration (FTLD) often overlaps clinically with corticobasal syndrome (CBS) and progressive supranuclear palsy (PSP), both of which have prominent eye movement abnormalities. 3 key findings →
Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source
Pick-type histology was seen in 14 cases (21%) and tau histological changes associated with frontotemporal dementia (FTD) linked to chromosome 17 (FTDP-17) were present in 11 cases (16%). 5 key findings →
Participants: 70 Evidence: low
Full summary, score breakdown and related studies → Original source
When corrected for multiple comparisons, patients with visual hallucinations had significantly greater disease duration, treatment duration, motor severity and complications, sleep disturbances, in particular excessive daytime somnolence and rapid eye movement sleep behavioural disorder, disorders of mood, autonomic dysfunction and global, frontal and visuoperceptive cognitive dysfunction. 3 key findings →
Participants: 94 Evidence: low
Full summary, score breakdown and related studies → Original source
The results indicate a pathophysiologic association between nigrostriatal dysfunction and occipital glucose metabolic reduction in PD. 3 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
We reviewed the polysomnograms (PSGs) of 292 consecutive patients with sleep disorders (Parkinson's disease (PD), n=19, other sleep disorders, n=273) to investigate the sensitivity and specificity of the clinical diagnosis of rapid eye movement behavior disorder (RBD) compared with polysomnographic diagnosis. 3 key findings →
Participants: 19 Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 2,823 studies in this tag that have a study page, 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.
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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 Where this research is being discussed: events