A blood test for Alzheimer's disease is now available for clinical use in persons with cognitive impairment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Reliable quantitative blood biomarkers are important in vascular dementia (VaD) because early diagnosis and therapeutic intervention are effective in preventing progression of dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A timely diagnosis of frontotemporal degeneration (FTD) is frequently challenging due to the heterogeneous symptomatology and poor phenotype-pathological correlation. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mass spectrometry (MS)-based protein identification via MALDI ToF/ToF showed that fibrinogen-β-chain (spot 64) and fibrinogen-γ-chain (spot 91) with differential expression ratio >1.5 were significantly upregulated (p < 0.05) in AD patients when compared to non-AD individuals. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
With emerging amyloid therapies, documentation of the patient's amyloid status to confirm the etiology of a clinical diagnosis is warranted prior to instituting amyloid-based therapy. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A systematic interpretation strategy could support accurate diagnosis and staging of AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurological condition that affects millions of individuals around the world and for which there are few effective therapies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Do MRI-based metrics of a CSF-dynamics disorder, disproportionately enlarged subarachnoid-space hydrocephalus (DESH), correlate with discordant amyloid biomarkers (low CSF β-amyloid 1-42, normal Aβ-PET scan)? 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) develops into dementia over a period of several years, during which subjective cognitive impairment (SCI) and mild cognitive impairment (MCI) can be used as intermediary diagnoses of increasing severity. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
For many years Alzheimer's disease (AD) was associated with the dementia stage of the disease, the tail end of a pathophysiological process that lasts approximately two decades. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Idiopathic normal pressure hydrocephalus (iNPH) is a neurological syndrome characterized by the clinical triad of gait disorder, cognitive impairment and urinary incontinence. 5 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
During the past ten years, over 5,000 cerebrospinal fluid (CSF) samples were analyzed at the Reference Center for Biological Markers of Dementia (BIODEM), UAntwerp, for core Alzheimer's disease (AD) CSF biomarkers: amyloid-β peptide of 42 amino acids (Aβ1-42), total tau protein (T-tau), and tau phosphorylated at threonine 181 (P-tau181P). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mild cognitive impairment (MCI) is a prevalent and complex condition among older adults that often progresses into Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) associated proteins exist in cerebrospinal fluid (CSF). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Systemic comorbidity precipitates the risk for dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
CSF α-synuclein levels were higher in AD patients as compared with cognitively healthy controls (P=.019) and patients with synucleinopathies (P<.001). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Early clinical symptoms of sporadic Creutzfeldt-Jakob disease (CJD) may overlap with other neurodegenerative diseases like Alzheimer's disease (AD) and frontotemporal degeneration (FTD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
We hypothesized that one mechanism underlying the association between obstructive sleep apnea (OSA) and Alzheimer's disease is OSA leading to decreased slow wave activity (SWA), increased synaptic activity, decreased glymphatic clearance, and increased amyloid-β. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (apoE) is associated with lipoproteins in the cerebrospinal fluid (CSF). 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
41/100
SMC ε4+ showed greater amyloid deposition than SMC ε4-, but no hypometabolism or medial temporal lobe (MTL) atrophy. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia, currently affecting 35 million people worldwide. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The treatment of complex and multifactorial diseases constitutes a big challenge in day-to-day clinical practice. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Excessive microglial activation might be a central pathological process in GRN-related frontotemporal dementia (FTD-GRN). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The timely detection of neurodegenerative diseases is central to improving clinical care as well as enabling the development and deployment of disease-modifying therapies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a leading cause of dementia, and the current diagnostic methods of AD, such as positron emission tomography imaging, have a high cost and poor accessibility. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
9 of the 3,322 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 9. The same 9 appear here every time.
- C-terminal neurogranin is increased in cerebrospinal fluid but unchanged in plasma in Alzheimer's disease
- APOE ɛ4 carriership determines a faster plasma p-tau217 progression in Aβ-positive individuals
- Obesity impacts brain metabolism and structure independently of amyloid and tau pathology in healthy elderly
- Plasma biomarkers of amyloid, tau & neuroinflammation in Alzheimer’s disease and corticobasal syndrome
- Potential association of bone mineral density loss with cognitive impairment and central and peripheral amyloid-β changes: a cross-sectional study
- Reference Intervals for Plasma Amyloid β in Korean Adults Without Cognitive Impairment
- Diagnostic value of fluid‐based non‐amyloid biomarkers for Alzheimer's disease and related dementias in a clinic‐based cohort from South Asia
- Race modifies the relationship between cognition and Alzheimer's disease cerebrospinal fluid biomarkers
- Transcranial blood-brain barrier opening in Alzheimer's disease patients using a portable focused ultrasound system with real-time 2-D cavitation mapping
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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 28,180 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.
What this library is — and isn't
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →