Diffusible, nonfibrillar ligands derived from Abeta1-42 are potent central nervous system neurotoxins.
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Summary
It is hypothesized that impaired synaptic plasticity and associated memory dysfunction during early stage Alzheimer's disease and severe cellular degeneration and dementia during end stage could be caused by the biphasic impact of Abeta-derived diffusible ligands acting upon particular neural signal transduction pathways.
- Type
- article
- Published
- 1998-05-26
- Cited by
- 3,697
- References
- 69
- Access
- Open access
- OpenAlex
- https://openalex.org/W2165021720
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:28329526
Keywords
Neuroprotection, Neurotoxicity, FYN, Neurotoxin, Neuroscience
References
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Cited by
- Molecular interaction between type 2 diabetes and Alzheimer’s disease through cross-seeding of protein misfolding
- In vitro studies of Flemish, Dutch, and wild-type beta-amyloid provide evidence for two-staged neurotoxicity.
- Pravastatin inhibits pro-inflammatory effects of Alzheimer's peptide Abeta(1-42) in glioma cell culture in vitro.
- A mechanism of macroscopic (amorphous) aggregation of the tobacco mosaic virus coat protein.
- Small assemblies of unmodified amyloid β-protein are the proximate neurotoxin in Alzheimer’s disease
- Soluble Aβ homeostasis in AD and DS: impairment of anti-amyloidogenic protection by lipoproteins
- Deposition of amyloid fibrils promotes cell-surface accumulation of amyloid beta precursor protein.
- NSAID and Antioxidant Prevention of Alzheimer's Disease: Lessons from In Vitro and Animal Models
- The Contribution of Microscopy to the Study of Alzheimer’s Disease, Amyloid Plaques and Aβ Fibrillogenesis
- Cyclooxygenase‐Dependent Lipid‐Modification of Brain Proteins
- Role of the 39-kDa receptor-associated protein (RAP) in Alzheimer's disease
- Tetracycline inhibits W7FW14F apomyoglobin fibril extension and keeps the amyloid protein in a prefibrillar, highly cytotoxic state
- Solvent and mutation effects on the nucleation of amyloid beta-protein folding.
- Biological applications of localised surface plasmonic phenomenae.
- Protective effects of EUK4010 on β‐amyloid(1–42) induced degeneration of neuronal cells
- Therapeutic approaches to Alzheimer's disease.
- Computer Simulations of Alzheimers Amyloid β-Protein Folding and Assembly
- The genetics and molecular pathology of Alzheimer's disease: roles of amyloid and the presenilins.
- Cystatin C reduces the in vitro formation of soluble Aβ1‐42 oligomers and protofibrils
- アミロイドβペプチド（Aβ）を標的とした人工タンパク質・ペプチドの設計とAβ集合体形成の制御
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