ArticlePrion2018
Somatostatin in Alzheimer's disease: A new Role for an Old Player.
Article in Prion, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 66 citations in OpenAlex.
- Forced treadmill running and ladder climbing physical activity attenuates cognitive decline and protein aggregates in aged 3xTg-AD mice.Molecular brain · 2026Article
- Somatostatin in Aging: Correlations with Selected Central Nervous System and Gastrointestinal Tract Diseases.International journal of molecular sciences · 2026Review
- Therapeutic Potential of Somatostatin and Its Analogues in Alzheimer's Disease: From Molecular Mechanisms to Preclinical Studies.Molecular neurobiology · 2026Review
- Brain peptides in Alzheimer's disease - pathophysiology and therapeutic advances.Cell and tissue research · 2026Review
- Molecular hallmarks of excitatory and inhibitory neuronal resilience to Alzheimer's disease.Molecular neurodegeneration · 2025Article
- The Primary Cilia are Associated with the Axon Initial Segment in Neurons.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Temporal ablation of the ciliary protein IFT88 alters normal brainwave patterns.Scientific reports · 2025Article
- Temporal Ablation of the Ciliary Protein IFT88 Alters Normal Brainwave Patterns.bioRxiv : the preprint server for biology · 2024Article
- Somatostatin: Linking Cognition and Alzheimer Disease to Therapeutic Targeting.Pharmacological reviews · 2024Review
- Somatostatin-SSTR3-GSK3 modulates human T-cell responses by inhibiting OXPHOS.Frontiers in immunology · 2024Article
- Influence of Alzheimer's disease related neuropathology on local microenvironment gene expression in the human inferior temporal cortex.GEN biotechnology · 2023Article
- Brain Hydrophobic Peptides Antagonists of Neurotoxic Amyloid β Peptide Monomers/Oligomers-Protein Interactions.International journal of molecular sciences · 2023Review
- Transition metal ions and neurotransmitters: coordination chemistry and implications for neurodegeneration.RSC chemical biology · 2023Review
- In-silico EEG biomarkers of reduced inhibition in human cortical microcircuits in depression.PLoS computational biology · 2023Article
- Predicting Key Genes and Therapeutic Molecular Modelling to Explain the Association betweenInternational journal of molecular sciences · 2023Article
- Somatostatin slows Aβ plaque deposition in aged APPScientific reports · 2023Article
- Conformational and functional changes of the native neuropeptide somatostatin occur in the presence of copper and amyloid-β.Nature chemistry · 2022Article
- Molecular origin of somatostatin-positive neuron vulnerability.Molecular psychiatry · 2022Article
- Assessing equivalent and inverse change in genes between diverse experiments.Frontiers in bioinformatics · 2022Article
- Bulk and Single-Nucleus Transcriptomics Highlight Intra-Telencephalic and Somatostatin Neurons in Alzheimer's Disease.Frontiers in molecular neuroscience · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The amyloid beta (Aβ) peptide is central to the pathogenesis of Alzheimer's disease (AD). Insights into Aβ-interacting proteins are critical for understanding the molecular mechanisms underlying Aβ-mediated toxicity. We recently undertook an in-depth in vitro interrogation of the Aβ1-42 interactome using human frontal lobes as the biological source material and taking advantage of advances in mass spectrometry performance characteristics. These analyses uncovered the small cyclic neuropeptide somatostatin (SST) to be the most selectively enriched binder to oligomeric Aβ1-42. Subsequent validation experiments revealed that SST interferes with Aβ fibrillization and promotes the formation of Aβ assemblies characterized by a 50-60 kDa SDS-resistant core. The distributions of SST and Aβ overlap in the brain and SST has been linked to AD by several additional observations. This perspective summarizes this body of literature and draws attention to the fact that SST is one of several neuropeptide hormones that acquire amyloid properties before their synaptic release. The latter places the interaction between SST and Aβ among an increasing number of observations that attest to the ability of amyloidogenic proteins to influence each other. A model is presented which attempts to reconcile existing data on the involvement of SST in the AD etiology.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.