28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
It is now widely accepted that the development of neurodegenerative diseases depends on and affects many pathological processes, both in the brain and the periphery. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebral amyloid angiopathy (CAA), which is prevalent among older adults, constitutes a major cause of brain hemorrhage, dementia, and cognitive decline. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Barnes Maze Acquisition was performed on males (N = 4-5/genotype) after habituation and several days training. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The precise regulation of DSCR gene expression is crucial to maintain the brain homeostasis, especially in those areas with high levels of gene expression associated with a remarkable process of learning and cognition. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The role of noise pollution as a risk factor for Alzheimer disease (AD) is unclear, with observational studies yielding conflicting results susceptible to confounding and reverse causality. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The onset and sustenance of Alzheimers and Parkinsons is solely dependent on the driving power of the immune cytokine interleukin-1 beta (IL-1β), arising from neuronal distress and release of sAPPα, which activates microglia for synthesis and release of IL-1β driving synthesis of βAPP, Aβ plaques and synthesis and activation of MAPKp38 for phosphorylation of tau for neurofibrillary tangle formation in Alzheimers and for a-synuclein for formation of Lewy bodies in Parkinsons. 1 key finding →
Evidence: low
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Alzheimer disease (AD) is a neurodegenerative disorder characterized by amyloid plaque deposition, neurofibrillary tangles, and chronic neuroinflammation. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Down syndrome (trisomy 21) is the most common genetic cause of intellectual disability. 1 key finding →
Design: narrative review Evidence: low
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Familial frontotemporal dementia (FTD) is a genetically heterogeneous disease with various clinical manifestations, making it difficult to diagnose. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In each case the framework recovered known disease genes and identified biologically coherent, disease-specific modules: in AD, 17 stable high-confidence genes and modules enriched in lipid and cholesterol metabolism and amyloid precursor protein processing; in PD, 17 stable genes and modules associated with mitophagy, ubiquitin-proteasome signaling, and mitochondrial dysfunction; in RA, 20 stable genes and modules enriched in antigen presentation and JAK-STAT cytokine signaling. 2 key findings →
Evidence: low
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Microglia are central regulators of Alzheimer's disease pathogenesis, but their roles cannot be reduced to a simple protective-versus-harmful dichotomy. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease currently has no cure and is usually detected too late for interventions to be effective. 3 key findings →
Evidence: low
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The 5' untranslated region (UTR) of the APP gene, encompassing 147 base pairs between the transcriptional (+1) and the translational start site, was examined for its role in APP expression. 4 key findings →
Evidence: low
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Gene dysregulation in trisomy 21 can cause disorders of genes that are members of the heat-shock proteins (HSPs) family and contribute to the early onset of Alzheimer's disease (AD) in Down syndrome (DS). 2 key findings →
Evidence: low
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Poly(ADP-ribosyl)ation (PARylation), a crucial post-translational modification, is catalyzed by ADP-ribosyltransferases (ARTs) and has significant implications in various cellular processes, including DNA damage response, cell signaling, and immune processes. 2 key findings →
Evidence: low
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Of note, using large-scale transcriptome and chromatin profiling, we show that T cell shape microglia-specific metabolic plasticity in both genetic and epigenetic resolution. 2 key findings →
Evidence: low
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Eight proteins were differently expressed in carriers with larger WMH volumes (Figure 1). 5 key findings →
Evidence: low
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Our findings support apathy and APOE ε4 as robust predictors of conversion to MCI and ADD, and demonstrate novel associations between antidepressant use and conversion. 3 key findings →
Evidence: low
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CWPs consist predominantly of two novel arrangements of type I Aβ filaments, and we have designated them as type Ic and type Id Aβ filaments. 5 key findings →
Evidence: low
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Here we present our research design and preliminary results in ADAD mutation carriers and controls. 5 key findings →
Evidence: low
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We identified an interaction between TDP-43 and APOE through immunoprecipitation followed by proteomics in mice, verified in human brain by co- immunoprecipitation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
It is associated with intracerebral hemorrhage (ICH), cognitive decline, and gait disturbance. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We evaluated known AD-associated loci (Bellenguez et al. 2022) and 27 loci reached nominal significance (p < 0.05) in at least one cognitive domain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
ADAM10 plays a fundamental role in brain function, and sufficient studies support its involvement in AD pathogenesis. 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 Free full text
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.
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 28,180 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.
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 →