We found that brain YKL-40 immunoreactivity was observed in a subset of astrocytes in all four diseases and in controls. 5 key findings →
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.
To study the potential diagnostic value of abnormally phosphorylated tau protein in Creutzfeldt-Jakob disease (CJD) compared to Alzheimer's disease (AD), we determined levels of tau phosphorylated at threonine 231 (p-tau231) and of total tau (t-tau) in cerebrospinal fluid (CSF) of CJD patients, AD patients, and healthy controls (HC). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Assay drift may reduce statistical power or even confound analyses. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuropsychological tests, CSF markers, and hippocampal volume predicted conversion from MCI to AD and general dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Familial Alzheimer's disease (AD) due to PSEN1 mutations provides an opportunity to examine AD biomarkers in persons in whom the diagnosis is certain. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent studies show that fibrinogen plays a role in the pathogenesis of Alzheimer's disease (AD), which may be crucial to neurovascular damage and cognitive impairment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Overall, these results support the vervet as a non-human primate model of amyloid-related neurodegeneration, such as Alzheimer's disease and cerebral amyloid angiopathy, and highlight Aβ 1-40 and p-tau 181 as potentially valuable biomarkers of these processes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the diagnosis of Alzheimer's disease (AD) total tau (T-tau), tau phosphorylated at threonine 181 (P-tau181), and the 42 amino acid isoform of alpha β-amyloid (Aβ) are well established surrogate CSF markers. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Between 1992 and 2000, 8 women developed dementia (4 AD, 3 vascular dementia, 1 mixed vascular dementia and AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Alzheimer's disease (AD) is a progressive neurodegenerative disease with cognitive dysfunction as its major clinical symptom. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although the use of cerebrospinal fluid (CSF) amyloid β1-42 (Aβ42), tau (T-tau), and phosphorylated tau (p-tau181) gives added diagnostic and prognostic values, the diffusion is still limited in clinical practice and only a restricted number of patients receive an integrated clinico-biological diagnosis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our results confirm the key role of CSF biomarkers in predicting patient conversion from MCI to dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Regulation of astrocytic mitochondrial function and redox status by IGF-1 is essential to maintain astrocytic function and coordinate hippocampal-dependent spatial learning. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Saito et al developed a novel amyloid precursor protein (APP) knock-in mouse model (APP NL-G-F ) for Alzheimer's disease (AD) to overcome the problem of overexpression of APP in available transgenic mouse models. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
The development of blood-based biomarkers of Alzheimer's disease (AD) pathology as tools for screening the general population, and as the first step in a multistep process to determine which non-demented individuals are at greatest risk of developing AD dementia, is essential. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Myeloperoxidase (MPO) is a key enzyme in inflammatory and degenerative processes, although conflicting reports have been presented concerning its expression in the brain. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study evaluated the neuroprotective and neuroimmunomodulatory potential of apigenin using in vitro models of neuroinflammation associated with AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Amyloid-β (Aβ) oligomers largely initiate the cascade underlying the pathology of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Prolonged intake of excessive amounts of ethanol is known to have adverse effects on the central nervous system (CNS). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
FTS•B effectively counteracted cognitive decline by regulating neuroinflammation via NF-κB signaling in APP/PS1 mice, providing preliminary experimental evidence that FTS•B is a promising therapeutic agent in AD treatment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The present study was designed to follow neuroinflammation after ischemic brain injury in the long-term survival rat model. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
CSF neurofilament contributes to a panel of CSF α-synuclein species in differentiating PD patients from healthy controls. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cumulative evidence shows that modifications in lifestyle factors constitute an effective strategy to modulate molecular events related to neurodegenerative diseases, confirming the relevant role of epigenetics. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings provide further evidence for the roles of hypothalamic and metabolic dysfunction in AD, which in the 3xTg-AD mouse model appears to be dependent on both sex and diet. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The implication of epigenetic mechanisms in Alzheimer's disease (AD) has been demonstrated in several studies. 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 →