28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
This study was a retrospective analysis of administrative data (20% sample) of 15 996 Medicare Part D enrollees who received a DES in 2006 to 2007. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A total of 143 patients with cognitive concerns were included who underwent a PrecivityAD2 test as part of their clinical evaluation. 5 key findings →
Participants: 4,000 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Although β-site APP-cleaving enzyme 1 (BACE1) and secretase inhibitors did not achieve success in clinical trials because of mechanism-based toxicity and cognitive impairment, new monoclonal antibodies such as lecanemab and donanemab have shown high amyloid plaque clearance and reduced cognitive deterioration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer′s disease (AD) is a chronic neurodegenerative disorder that leads to memory loss and changes in mental and behavioral functions in elderly individuals. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder marked by memory loss, cognitive decline, and behavioral changes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Despite substantial investment in biomedical and pharmaceutical research over the past two decades, the global prevalence of Alzheimer's disease (AD) and AD-related dementias (AD/ADRD) is still rising. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Frontotemporal dementia (FTD) encompasses a broad, clinically and neuropathologically diverse group of neurodegenerative disorders associated with changes in personality, behaviour, and/or language due to the progressive degeneration of the frontal and temporal lobes of the brain. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Tau mutant cortical organoids showed altered mitochondrial function and gene expression related to neuronal development, with synaptic markers and neuronal activity reduction. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In addition to the core clinical features of fluctuating cognition, visual hallucinations, and parkinsonism, individuals with dementia with Lewy bodies (DLB) frequently experience chronic and debilitating major depression. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The repeated inability of Aβ therapies to pass clinical tests in sporadic AD points to the complexity of the disease and indicates that earlier or more interventions could be necessary. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The first search utilized the following MeSH terms and keywords: ‘Plasma Exchange’, ‘Plasmapheresis’, ‘Therapeutic plasma exchange’, ‘Apheresis’, ‘Aβ’, ‘p-tau’, ‘Total-tau’, ‘Alzheimer's disease’, ‘Cognitive dysfunction’, ‘neurodegenerative diseases’, ‘centrifugation’, ‘membranous’, and ‘filtration’ in the Title/Abstract, yielding 146 results. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In a cohort of 75 patients who completed Moneta's program (average age 73 ± 10, average MoCA score 20 ± 5), 59% had MCI and 33% had dementia. 5 key findings →
Participants: 75 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD), the most prevalent form of dementia, is pathologically defined by amyloid-β (Aβ) plaques, neurofibrillary tangles, synaptic loss, and progressive neuronal degeneration. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
For diverse neurodegenerative disorders, microglial cells are activated. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Depression in Alzheimer's disease (AD) dementia has become an increasingly recognized public health concern due to its high prevalence and substantial impact on patient outcomes. 5 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
One of the major consequences of diabetes mellitus that has gained attention due to its rising incidence is cognitive impairment. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mixed dementia (MD), characterized by overlapping features of Alzheimer's disease (AD) and vascular dementia (VaD), represents the most prevalent form of late-life cognitive decline. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Vascular dementia (VaD) is a leading cause of cognitive decline and arises from heterogeneous cerebrovascular pathologies, most commonly cerebral small vessel disease and chronic cerebral hypoperfusion. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
and neurogranin changes correlated with sabirnetug-AβO target engagement (p ≤ 0.01). 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is characterized by the formation of extracellular amyloid plaques containing the amyloid β-protein (Aβ) within the parenchyma of the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD)-a complex disease showing multiple pathomechanistic alterations-is triggered by nonlinear dynamic interactions of genetic/epigenetic and environmental risk factors, which, ultimately, converge into a biologically heterogeneous disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Investigations of apolipoprotein E (APOE) gene, the major genetic risk modifier for Alzheimer's disease (AD), have yielded significant insights into the pathogenic mechanism. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive degenerative neurological disorder affecting nearly one in nine elderly people in the United States. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (APOE) is the major cholesterol carrier in the brain, affecting various normal cellular processes including neuronal growth, repair and remodeling of membranes, synaptogenesis, clearance and degradation of amyloid β (Aβ) and neuroinflammation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disease that causes chronic cognitive dysfunction. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 3,106 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.
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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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.
1,034 records (3.6% 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 →