Our findings highlight the potential of serum NfL as a useful surrogate end point of disease severity in upcoming targeted treatments. 3 key findings →
Evidence: moderate
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.
In view of the paucity of data on cerebrospinal fluid (CSF) biomarkers in Chinese patients, we evaluated the validity of tau, phosphorylated tau 181 (p-tau-181), amyloid β 42 (Aβ42), and Aβ40 proteins in Chinese patients with Alzheimer's disease (AD). 3 key findings →
Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
Animal models of disease are valuable resources for investigating pathogenic mechanisms and potential therapeutic interventions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dysfunction of the blood-brain barrier is more prominent in white-matter lesions seen in ischemic CVD than in AD and may have a role in the pathogenesis of cerebrovascular white-matter lesions. 3 key findings →
Participants: 14 Evidence: low
Full summary, score breakdown and related studies → Original source
Histone acetylation is an epigenetic modification that plays a critical role in chromatin remodelling and transcriptional regulation. 4 key findings →
Participants: 14 Evidence: low
Full summary, score breakdown and related studies → Original source
The MWM results showed that electroacupuncture improves the escape latency time and the swimming distance of AD rats. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In summary, high (11)C-Pittsburgh Compound B positron emission tomography retention significantly correlates with both fibrillar β-amyloid and losses of neuronal nicotinic acetylcholine receptor subtypes at autopsy, suggesting a closer involvement of β-amyloid pathology with neuronal nicotinic acetylcholine receptor subtypes than with inflammatory processes. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
We measured tau concentrations in cerebrospinal fluid (CSF) samples taken during the lifetime of 43 patients with Alzheimer's disease (AD) and correlated these values with neurofibrillary tangle (NFT) scores as well as glial fibrillary acidic protein (GFAP) expression as a marker of astrocytosis in the brain post-mortem. 1 key finding →
Participants: 43 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is increasingly prevalent worldwide, and disease-modifying treatments may soon be at hand; hence, now, more than ever, there is a need to develop techniques that allow earlier and more secure diagnosis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The pathological alterations in Binswanger's diseased brains include regressive changes in the astroglia and activation of the microglia with a decrease in the oligodendroglia, which were associated with the degradation of both myelin and axonal components. 5 key findings →
Participants: 17 Evidence: low
Full summary, score breakdown and related studies → Original source
HIV-associated neurocognitive disorders (HAND) affect up to 50 % of HIV-infected adults, independently predict HIV morbidity/mortality, and are associated with neuronal damage and monocyte activation. 4 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
We conclude that reducing ApoE4 levels should be explored further as a therapeutic approach for APOE4 carriers with tauopathy including Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Insulin significantly improved cognitive and memory functions in VD model rats ( p < 0.05). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
To gain insight of the underlying mechanisms of astroglial response to Alzheimer's disease (AD), the level of glial fibrillary acidic protein (GFAP) in cerebrospinal fluid (CSF) from controls and AD subjects were immunochemically determined, and the correlation between that level and dementia severity of AD patients was evaluated. 3 key findings →
Participants: 13 Evidence: low
Full summary, score breakdown and related studies → Original source
Astrocytes are one of the brain's major cell types and are responsible for maintaining neuronal homeostasis via regulating the extracellular environment, providing metabolic support, and modulating synaptic activity. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Altered concentrations of two out of three MMPs investigated in this study suggest that this family of biomolecules may play a role in the AD pathophysiology. 3 key findings →
Participants: 33 Evidence: low
Full summary, score breakdown and related studies → Original source
There is an association between plasma GFAP and regional 18F-SMBT-1 PET, and this association appears to be dependent on brain Aβ load. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings suggest that VILIP-1 may play a role in the AD pathophysiology and is a good candidate for dynamic biomarker of AD, although this issue requires further investigation. 3 key findings →
Participants: 33 Evidence: low
Full summary, score breakdown and related studies → Original source
Depressed individuals are twice as likely to develop Alzheimer's disease (AD) as compared to controls. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid-β (Aβ) fibrils in neuritic plaques are a hallmark of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Gait disturbances are some of the earliest changes in dementia and their monitoring presents an opportunity for early diagnosis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma amyloid β-42 (Aβ42) and Aβ42/Aβ40 are increasingly recognized as biomarkers for dementia, with low levels indicating increased risk. 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
CD22 has been suggested to contribute to Alzheimer's disease (AD) pathogenesis by inhibiting microglial amyloid β (Aβ) phagocytosis. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
KRG administration showed the Lactobacillus dominance in the gut microbiota. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of cognitive decline worldwide, occurring in about 10% of people older than 65 years. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 →