Blood-based biomarkers hold significant promise for the early detection and diagnosis of Alzheimer’s disease (AD) and other dementias. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Blood-based biomarkers hold significant promise for the early detection and diagnosis of Alzheimer’s disease (AD) and other dementias. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent advances in dementia research have expanded our understanding of modifiable risk factors, with air pollution being a well-established contributor. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
• The new CB 2 antagonist PGN36 is able to cross the Blood-Brain Barrier. • PGN36 treatment effectively alleviates TAU P301L -induced cognitive decline . • PGN36 is able to reduce TAU protein expression levels and restore synaptic plasticity. • PGN36 modulates TAU P301L -induced pyroptosis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The developmental origin of Alzheimer disease (AD) has been proposed but is arguably debated. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This diploma thesis presents the work carried out during 6 months within the Laboratory directed by Professor Millet, written under the supervision and with the support of Dr. Benjamin Tournier and Silvia Braconi Quintaje. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) affects over 55 million people worldwide and lacks effective disease-modifying therapies targeting neuroinflammation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Emerging evidence indicates that globus pallidus (GP) function can be modulated by orexin-A in movement disorders, while its role in Alzheimer’s disease (AD) and dementia with Lewy bodies (DLB) remains unclear. 4 key findings →
Participants: 25 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Compared with stage 0 CKM syndrome, stages 3 and 4 were significantly associated with an increased risk of dementia (hazard ratio [HR], 1.35; 95% confidence interval [CI], 1.14-1.59; HR, 1.80; 95% CI 1.57-2.07). 5 key findings →
Participants: 389,287 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Semantic dementia (SD) is a clinical subtype of frontotemporal dementia characterized by impaired word comprehension and semantic memory, and occurs nearly always sporadically. 1 key finding →
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
While neuropathological and genetic studies have established the crucial involvement of TDP-43 proteinopathy in the pathogenesis of amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and related neurodegenerative disorders, multiple studies have described the presence of TDP-43 inclusions in muscular disorders, including inclusion body myositis but also other related rimmed vacuole myopathies. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Frontotemporal dementia (FTD) is a group of early onset and progressive disorders, characterized by degeneration in the frontal and temporal lobes, and subsequent deterioration in cognition, personality, social behavior, and language, with aggregates of the RNA-binding protein TDP-43 being present in ~45% of the cases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
TDP-43 and FUS are RNA-binding proteins involved in the regulation of diverse RNA-processing events and have been strongly implicated in neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Inter-organelle contact sites are key hubs for organelle bidirectional crosstalk. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
86.8% of patients in this cohort presented more than one pathology. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Natural products (NPs) are considered to be the oldest medicine in human history and numerous NPs have been investigated to search for therapeutic agents in various diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is an age-associated neurodegenerative disorder with a complex etiology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BackgroundAlzheimer's disease (AD) causes cognitive function disorder and has become the preeminent cause of dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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
LAPs contained five monosaccharides. LAPs improved cognitive function and increased the number of Nissl bodies, lactate secretion, the IL-10 content, the relative fluorescence intensity of the IBA1 and AXL proteins, and the protein expression levels of AXL, Mertk, Glut1, HK2, PI3K, p-Akt/Akt, p-mTOR/mTOR and HIF-1α of immune-tolerant AD mice. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
SGLT2i empagliflozin and dapagliflozin exhibited neuroprotective actions against human Aβ 1–42 -induced neurotoxicity. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Autophagic markers beclin 1, LC3II and p62, and lysosome-related marker cathepsin B, all upregulated in AD astrocytes, were significantly reduced, while autophagic flux was rescued, by stabilizing 20 nm-MERCS. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1) is a critical deubiquitinating enzyme that is highly expressed in the central nervous system, where it participates in protein degradation and turnover as part of the ubiquitin-proteasome system (UPS). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
AMS-17 treatment improved cognitive function, enhanced blood-brain barrier (BBB) integrity, and promoted remyelination in VaD mice. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Vascular cognitive impairment and dementia (VCID) encompasses a heterogeneous group of disorders in which cerebrovascular pathology contributes to cognitive decline. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
10 of the 6,970 studies in this tag that have a study page, 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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →