The NLRP3 inflammasome pathway destroys neuronal cells primarily through the production of IL-18 and IL-1β. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
The NLRP3 inflammasome pathway destroys neuronal cells primarily through the production of IL-18 and IL-1β. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Vascular dementia (VD), characterized by cognitive decline and behavioral disorders, has seen a rapid increase in prevalence in recent years. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Frontotemporal dementia (FTD) refers to a group of neurodegenerative disorders characterized clinically by behavioral disturbances and pathologically by frontal and anterior temporal lobe neurodegeneration, resulting in brain atrophy. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
High Resolution Image Download MS PowerPoint Slide Pathological aggregates of TDP-43 are implicated in Alzheimer’s disease, frontotemporal dementia, and amyotrophic lateral sclerosis. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neuronal cytoplasmic aggregation and nuclear depletion of the TAR DNA-binding protein 43 (TDP-43) is the most characteristic pathology of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), causing toxicity through cytoplasmic gain and nuclear loss of function mechanisms. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Primary and secondary tauopathies are major causes of dementia characterized by the abnormal accumulation of microtubule-associated protein tau. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neurodegenerative diseases are currently among the most devastating diseases with no effective disease-modifying drugs in the market, with Alzheimer's disease (AD) being the most prevalent. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the leading cause of dementia worldwide and represents a growing public health challenge in aging societies. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In the dementia scenario, 26.9% of participants preferred unlimited medical treatment. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Poststroke cognitive impairment (PSCI) refers to any level of cognitive decline occurring after a stroke, ranging from mild to severe impairments, while PSCI with dementia describes a more severe form where the cognitive decline significantly affects daily functioning and meets the clinical criteria for dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Anti-amyloid monoclonal antibodies (lecanemab and donanemab) represent the first disease-modifying therapies for early symptomatic Alzheimer's disease (AD)- Italy's National Health Service (SSN) must determine whether to include these therapies within Essential Levels of Care (LEA), requiring reimbursement across all regions. 5 key findings →
Participants: 42,000 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive accumulation of toxic amyloid species. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Each year, the French independent bulletin Prescrire publishes a list of medicines, "Drugs to avoid", that should not be used in clinical practice as their risk-to-benefit ratio is unfavourable. 1 key finding →
Participants: 50,000 Evidence: low
Full summary, score breakdown and related studies → Original source
AAV-mediated progranulin delivery reduced lipofuscinosis in Grn -/- mice even after the onset of pathology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia worldwide. β-amyloid peptide (Aβ) is currently assumed to be the main cause of synaptic dysfunction and cognitive impairments in AD, but the molecular signaling pathways underlying its neurotoxic consequences have not yet been completely explored. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aggregates of the microtubule-associated protein tau are a defining feature of several neurodegenerative diseases that are collectively known as tauopathies, and constitute one of the hallmark lesions of Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Emerging evidence indicates that moderate intensity aerobic exercise is positively correlated with cognitive function and memory. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Impaired glucose metabolism, decreased levels of thiamine and its phosphate esters, and reduced activity of thiamine-dependent enzymes, such as pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase and transketolase occur in Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
All people want to age "successfully," maintaining functional capacity and quality of life as they reach advanced age. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cognitive dysfunction is common in Parkinson's disease (PD) and predicts poor clinical outcomes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Since its discovery some hundred years ago, Alzheimer's disease (AD), a neurodegenerative disease and an eminent cause of most dementia, continues to pose problems for affected families and society, especially in developed countries. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dysfunction of the autonomic nervous system afflicts most patients with Parkinson disease and other synucleinopathies such as dementia with Lewy bodies, multiple system atrophy, and pure autonomic failure, reducing quality of life and increasing mortality. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal dementia (FTD) encompasses a spectrum of clinical syndromes characterized by progressive executive, behavioural and language dysfunction. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the sample studied, music therapy improved some cognitive, psychological, and behavioural alterations in patients with Alzheimer disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The evidence about the role the designed and built environment plays in supporting individuals living with dementia has been steadily mounting for almost 40 years. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
9 of the 3,475 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 9. The same 9 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 28,980 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 28,980 records, built mostly from automated pulls of Europe PMC (62.8% of the library) and OpenAlex (17.6%), 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.
1,038 records (3.6% of the library) are not peer-reviewed — 966 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 →