The pathogenesis of white matter lesions, which are frequently found in ischemic cerebrovascular disease and Alzheimer's disease, remains unclear. 3 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.
Both protein kinases and phosphoprotein phosphatases are important components of signal transduction systems in cells. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our data suggest that the association between neuroinflammation and AD is stronger in relatively young patients than in the oldest patients. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The retired players' ages averaged 45.6 ± 8.9 years (range, 30-60 years), and they had 6.8 ± 3.2 years (maximum, 14 years) of NFL play. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Chronic neuroinflammation is now considered one of the major factors in the pathogenesis of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) biomarkers T-Tau and Aβ(42) are linked with Alzheimer's disease (AD), yet little is known about the relationship between CSF biomarkers and structural brain alteration in healthy adults. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
IIS is functional in astrocytes. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
Alzheimer's disease is one of the most common causes of death worldwide, with poor treatment options. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease (AD), one of the early responses to Aβ amyloidosis is recruitment of microglia to areas of new plaque. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Among the different signaling molecules released during reactive gliosis occurring in Alzheimer's disease (AD), the astrocyte-derived S100B protein plays a key role in neuroinflammation, one of the hallmarks of the disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Formalin-fixed brain specimens from sporadic cases with frontotemporal dementia (eight with tau-positive Pick bodies, five with frontotemporal lobar degeneration without inclusions) were compared with those from non-diseased controls (n = 5). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Advances in the development of three-dimensional (3D) brain organoids maintained in vitro have provided excellent opportunities to study brain development and neurodegenerative disorders, including Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
CD2-Associated Protein affects Aβ levels and Aβ42/Aβ40 ratio in vitro. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The 3xTg-AD mouse develops a progressive Alzheimer's disease- (AD-) like brain pathology that causes cognitive- and neuropsychiatric-like symptoms of dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer disease (AD) is characterized by progressive memory loss, reduction in cognitive functions, and damage to the brain. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings identify Syt1 as a novel Ca(2+)-sensitive PS1 modulator that could regulate synaptic Aβ, opening avenues for novel and selective synapse targeting therapeutic strategies. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the primary cause of dementia in the elderly. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This demonstrates that an AD-like APP processing, yielding to levels of APP, βCTF and Aβ42/Aβ40 ratio similar to those observed in AD patients, are sufficient to rapidly trigger early steps of the amyloidogenic and Tau pathways in vivo. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The characteristic neuropathological changes associated with Alzheimer's disease (AD) and other lines of evidence support the amyloid cascade hypothesis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Formation of Aβ oligomers and fibrils plays a central role in the pathogenesis of Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Label-free simultaneous detection of Alzheimer's disease (AD) specific biomarkers Aβ40 and Aβ42 peptides on a single platform using polypyrrole nanoparticle-based chemiresistive biosensors is reported here. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The RNA binding protein ELAVL4/HuD regulates the translation and splicing of multiple Alzheimer's disease (AD) candidate genes. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
CSF and blood-based biomarkers can evaluate for a range of neurologic disorders that are associated with dementia, including AD. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a debilitating dementia characterized by progressive memory loss and aggregation of amyloid-β (Aβ) protein into amyloid plaques in patient brains. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This data provides evidence that the PSEN1 mutations L286V and R278I significantly alter protein expression associated with AβPP processing and cellular redox status. 4 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 →