30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
These findings suggest that there is reduced chaperone-mediated autophagy activity in the PD brain, provide evidence for the role of autophagy in PD pathogenesis and Lewy body formation, and suggest that this pathway may be a suitable therapeutic target in PD. 3 key findings →
Evidence: low
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In the present study we describe an ELISA to quantify the light subunit of the neurofilament triplet protein (NFL) in CSF. 2 key findings →
Evidence: low
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The presynaptic protein alpha-synuclein is a prime suspect for contributing to Lewy pathology and clinical aspects of diseases, including Parkinson's disease, dementia with Lewy bodies, and a Lewy body variant of Alzheimer's disease. alpha-Synuclein accumulates in Lewy bodies and Lewy neurites, and two missense mutations (A53T and A30P) in the alpha-synuclein gene are genetically linked to rare familial forms of Parkinson's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
To better understand the pathogenesis of brain dysfunction in Gaucher disease (GD), we studied brain pathology in seven subjects with type 1 GD (four also exhibited parkinsonism and dementia), three with type 2 GD and four with type 3 GD. 3 key findings →
Evidence: low
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Mutations in the microtubule-associated protein tau, including P301L, are genetically coupled to hereditary frontotemporal dementia with parkinsonism linked to chromosome 17. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Pathogenic alpha-synuclein (alphaS) gene mutations occur in rare familial Parkinson's disease (PD) kindreds, and wild-type alphaS is a major component of Lewy bodies (LBs) in sporadic PD, dementia with LBs (DLB), and the LB variant of Alzheimer's disease, but beta-synuclein (betaS) and gamma-synuclein (gammaS) have not yet been implicated in neurological disorders. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Pathogenic changes in the brain of a PARK2 patient were recapitulated using iPSC technology. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
TDP-43 is a DNA/RNA-binding protein implicated in multiple steps of transcriptional and post-transcriptional regulation of gene expression. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
TDP-43, or TAR DNA-binding protein 43, is a pathological marker of a spectrum of neurodegenerative disorders, including amyotrophic lateral sclerosis and frontotemporal lobar degeneration with ubiquitin-positive inclusions. 2 key findings →
Evidence: low
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Many neurodegenerative proteinopathies share a common pathogenic mechanism: the abnormal accumulation of disease-related proteins. 4 key findings →
Evidence: low
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Parkinson's disease (PD) is a complex syndrome for which there is no disease-modifying treatment on the market. 4 key findings →
Evidence: low
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[(11)C](R)PK11195-PET measures upregulation of translocator protein, which is associated with microglial activation, [(11)C]PIB-PET is a marker of amyloid, while [(18)F]FDG-PET measures cerebral glucose metabolism (rCMRGlc). 4 key findings →
Evidence: low
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Parkinson's disease (PD) has been associated with mild cognitive impairment (PDMCI) and with dementia (PDD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Patients with Parkinson's disease (PD) often have cognitive deficits from the time of diagnosis. 4 key findings →
Evidence: moderate
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Reductions in cholinergic function occur in Alzheimer disease (AD) and dementia with Lewy bodies and correlate with cognitive decline. 4 key findings →
Participants: 89 Evidence: moderate
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We investigated consecutive patients with dementia. 4 key findings →
Participants: 536 Evidence: low
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Affect sharing and prosocial motivation are integral parts of empathy that are conceptually and mechanistically distinct. 4 key findings →
Participants: 275 Evidence: low
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There is growing evidence of activated microglia and inflammatory processes in the cerebral cortex in amyotrophic lateral sclerosis (ALS). 4 key findings →
Evidence: low
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Amyotrophic lateral sclerosis (ALS) is a degenerative disorder that is characterized by loss of motor neurons and shows clinical, pathological, and genetic overlap with frontotemporal dementia (FTD). 3 key findings →
Evidence: low
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Our data show changes in innate immune cells in MCI-LB compared to healthy controls in this small exploratory study. 5 key findings →
Design: cohort study Participants: 64 Evidence: moderate
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Participants in the study had an average age of 85.4 ± 7.1 years. 5 key findings →
Design: cross-sectional Evidence: low
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The early and accurate diagnosis of Alzheimer's Disease and Frontotemporal Dementia remains a critical challenge, particularly with traditional machine learning models which often fail to provide transparency in their predictions, reducing user confidence and treatment effectiveness. 5 key findings →
Evidence: low
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Lewy body dementia is the second most common form of neurodegenerative dementia, following Alzheimer's disease. 5 key findings →
Evidence: low
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In bvFTD patients, longer interoceptive-ACWs than controls were observed in the bilateral fronto-temporal and parietal regions. 5 key findings →
Evidence: low
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We show reduced fiber cross-section in LBD versus PD, and increased concentrations of plasma neurofilament light chain and p-tau217; with p-tau217 and fiber cross-section associated with cognition. 5 key findings →
Participants: 47 Evidence: low
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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