27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
We estimated the overall concentration (mean standardized values) and principal components (PCs) of the proteomics and lipidomics data independently. 5 key findings →
Participants: 1,372 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The study highlights the potential of integrating 18 F-FDG-PET with CSF biomarkers to improve the diagnosis, prognosis, and monitoring of AD, emphasizing the complexity and regional specificity of biomarker interactions in neurodegeneration. 1 key finding →
Participants: 90 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among 42 participants (median age: 71 years, 66.7% female), 26 (61.9%) were classified as progressors. 5 key findings →
Participants: 42 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cognitive assessment and analysis of plasma biomarkers are lower-cost options for the early assessment of Alzheimer's disease (AD). 1 key finding →
Participants: 327 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A total of 156 patients were clinically diagnosed with dementia based on the 2011 NIA-AA criteria, regardless of specific disease etiology, and all exhibited significant brain atrophy on anatomical magnetic resonance imaging (MRI), indicating neuronal injury (N+). 5 key findings →
Participants: 156 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
TDP-43 seeding activity was detected in 67% of TDP-43-linked symptomatic patients, with a specificity of 93%. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our results suggest that microglial activation is a major phenomenon linking Aβ and astrocyte reactivity in the living AD brain. 5 key findings →
Participants: 62 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) and dementia with Lewy bodies (DLB) are the two most common forms of dementia due to neurodegeneration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Individual biomarkers significantly predict decline across multiple cognitive domains. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Plasma Aβ levels and regional WMH burden are associated with glymphatic dysfunction as indicated by reduced ALPS. 3 key findings →
Participants: 216 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
APOE ε4 is associated with accelerated progression of AD pathology. 3 key findings →
Participants: 575 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We performed a retrospective analysis of the patients assessed at our memory unit for whom Alzheimer disease (AD) cerebrospinal fluid biomarker results were available. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common cause of dementia in the elderly. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Heterozygous, loss-of-function mutations in the granulin gene (GRN) encoding progranulin (PGRN) are a common cause of frontotemporal dementia (FTD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a multifactorial, age-related neurological disease characterized by complex pathophysiological dynamics taking place at multiple biological levels, including molecular, genetic, epigenetic, cellular and large-scale brain networks. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Current biomarkers used in research and in clinical practice in Alzheimer's Disease (AD) are the analysis of cerebral spinal fluid (CSF) to detect levels of Aβ42 and phosphorylated-tau, amyloid and FDG-PET, and MRI volumetry. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
β-Amyloid (Aβ) plaque deposition and neurodegeneration within temporoparietal and hippocampal regions may indicate increased risk of Alzheimer's disease (AD). 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
The links between β-amyloid (Aβ) and tau in Alzheimer's disease are unclear. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
An accurate and early diagnosis of Alzheimer's disease (AD) is important to select optimal patient care and is critical in current clinical trials targeting core AD neuropathological features. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Principle component analyses identified 3 factors: trophic (BDNF, VEGF, TGFβ), degenerative (GFAP, NfL), and inflammatory (TNFα, IL-6, IP-10, IL-10). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Following the development of the first methods to measure the core Alzheimer's disease (AD) cerebrospinal fluid (CSF) biomarkers total-tau (T-tau), phosphorylated tau (P-tau) and the 42 amino acid form of amyloid-β (Aβ42), there has been an enormous expansion of this scientific research area. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Subcortical small-vessel disease (SSVD) is a disorder well characterized from the clinical, imaging, and neuropathological viewpoints. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD), a primary cause of dementia globally, is traditionally diagnosed via cerebrospinal fluid (CSF) measures and positron emission tomography (PET). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Sleep deprivation can lead to an elevation of plasma Aβ40 and decrease of the Aβ42/Aβ40 ratio. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The complement system plays critical roles in development, homeostasis, and regeneration in the central nervous system (CNS) throughout life; however, complement dysregulation in the CNS can lead to damage and disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 3,069 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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 (3.7% 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 →