The results suggest that Tph2 inactivation influences AβPP processing, at least in the hippocampus, although levels of Aβ are unchanged. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Based on the hypothesis that tau is cleaved proteolytically and then released into the blood, we here provide evidence for the presence of an ADAM10-generated tau fragment (Tau-A) in serum. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Previous mass spectrometry analysis of cerebrospinal fluid (CSF) has allowed the identification of a panel of molecular markers that are associated with Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurodegenerative disorder characterized clinically by the progressive decline of memory and cognition. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease pathology is closely connected to the processing of the amyloid precursor protein (APP) resulting in the formation of a variety of amyloid-beta (Aβ) peptides. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We developed a sensitive method to analyze SNAP-25 levels in individual CSF samples that to our knowledge was not possible previously. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A resolution pathway exists in the brain and the alterations described herein strongly suggest a dysfunction of this pathway in AD. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disease that is pathologically characterized by extracellular deposition of beta-amyloid peptide (Abeta) and intraneuronal accumulation of hyperphosphorylated tau protein. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is multifactorial and apparently involves several different etiopathogenic mechanisms. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuroinflammation, especially innate immunocyte-mediated neuroinflammation, has been reported to participate in pathogenesis of Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Brain is one of the richest organs in lipid content. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is an age-associated neurodegenerative disorder with multifactorial etiology, intersecting genetic and environmental risk factors, and a lack of disease-modifying therapeutics. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
Alzheimer's disease (AD) is a progressive and synaptic failure disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
Apolipoprotein E4 (APOE4) is the greatest known genetic risk factor for developing sporadic Alzheimer's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
The apolipoprotein E ε4 gene is the most important genetic risk factor for sporadic Alzheimer's disease, but the link between this gene and neurodegeneration remains unclear. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The epsilon4 allele of apolipoprotein E (ApoE) is an important genetic risk factor for Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Since the genome-wide association studies in Alzheimer's disease have highlighted inflammation as a driver of the disease rather than a consequence of the ongoing neurodegeneration, numerous studies have been performed to identify specific immune profiles associated with healthy, ageing, or diseased brain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies and functional genomics studies have linked specific cell types, genes, and pathways to Alzheimer's disease (AD) risk. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the current study, we used a novel single-cell whole genome sequencing (scWGS) approach to assess aneuploidy in isolated neurons from the frontal cortex of normal control individuals (n = 6) and patients with AD (n = 10). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Several proteins have been linked to neurodegenerative disorders (NDDs), but their molecular function is not completely understood. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuropathological studies have revealed the presence of a broad variety of inflammation-related proteins (complement factors, acute-phase proteins, pro-inflammatory cytokines) in Alzheimer's disease (AD) brains. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common neurodegenerative disorder where the accumulation of amyloid plaques and the formation of tau tangles are the prominent pathological hallmarks. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
Genome-wide association studies demonstrated that polymorphisms in the CD33/sialic acid-binding immunoglobulin-like lectin 3 gene are associated with late-onset Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Chronic activation of the complement system and induced inflammation are associated with neuropathology in Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The small, calcium-sensor protein, calmodulin, is ubiquitously expressed and central to cell function in all cell types. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 8,203 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.
- Exploring the Therapeutic Potential of Chalcones in Alzheimer’s Disease: Mechanistic Insights and SAR Perspectives
- S-nitrosylation of parkin regulates ubiquitination and compromises parkin's protective function
- Developmental and aging changes in the expression patterns of beta-amyloid in the brains of normal and Down syndrome cases
- Rapid doubling of Alzheimer's amyloid-β40 and 42 levels in brains of mice exposed to a nickel nanoparticle model of air pollution
- Inflammatory markers and the risk of Alzheimer disease: the Framingham Study
- The many "Neurofaces" of Prohibitins 1 and 2: Crucial for the healthy brain, dysregulated in numerous brain disorders
- Synthesis and multitarget biological profiling of a novel family of rhein derivatives as disease-modifying anti-Alzheimer agents
- Exercise counteracts declining hippocampal function in aging and Alzheimer's disease
- The Effects of Chronic Exposure to Ambient Traffic-Related Air Pollution on Alzheimer's Disease Phenotypes in Wildtype and Genetically Predisposed Male and Female Rats
- Soluble TREM2 inhibits secondary nucleation of Aβ fibrillization and enhances cellular uptake of fibrillar Aβ
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 29,780 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 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), 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.
1,037 records (3.5% of the library) are not peer-reviewed — 964 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 →