Common Structure of Soluble Amyloid Oligomers Implies Common Mechanism of Pathogenesis

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Protofibrillar Intermediates of Amyloid β-Protein Induce Acute Electrophysiological Changes and Progressive Neurotoxicity in Cortical Neurons

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Fibrils Formed in Vitro from α-Synuclein and Two Mutant Forms Linked to Parkinson's Disease are Typical Amyloid

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Structural Studies of Amyloid Proteins at the Molecular Level

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A Potential Role of the Curry Spice Curcumin in Alzheimers Disease

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Assessing the Stability of Alzheimer’s Amyloid Protofibrils Using Molecular Dynamics

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Global Impairment of the Ubiquitin-Proteasome System by Nuclear or Cytoplasmic Protein Aggregates Precedes Inclusion Body Formation

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Prions: Protein Aggregation and Infectious Diseases

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Alzheimer brain-derived tau oligomers propagate pathology from endogenous tau

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Activation of Necroptosis in Multiple Sclerosis

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Antiparallel β-sheet: a signature structure of the oligomeric amyloid β-peptide

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Different Conformations of Amyloid β Induce Neurotoxicity by Distinct Mechanisms in Human Cortical Neurons

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Proteolytic Potential of the MSC Exosome Proteome: Implications for an Exosome-Mediated Delivery of Therapeutic Proteasome

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Small assemblies of unmodified amyloid $beta;-protein are the proximate neurotoxin in Alzheimer?s disease

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The Flavonoid Baicalein Inhibits Fibrillation of α-Synuclein and Disaggregates Existing Fibrils

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Aggregation promoting C-terminal truncation of α-synuclein is a normal cellular process and is enhanced by the familial Parkinson's disease-linked mutations

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Aggregated Tau activates NLRP3–ASC inflammasome exacerbating exogenously seeded and non-exogenously seeded Tau pathology in vivo

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Hsp104 Catalyzes Formation and Elimination of Self-Replicating Sup35 Prion Conformers

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NEURODEGENERATIVE DISEASES: New Concepts of Pathogenesis and Their Therapeutic Implications

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Atomic-resolution dynamics on the surface of amyloid-β protofibrils probed by solution NMR

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Molecular Mechanisms of Amyloid Oligomers Toxicity

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Increased β-Cell Apoptosis Prevents Adaptive Increase in β-Cell Mass in Mouse Model of Type 2 Diabetes

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Stabilization of a β-hairpin in monomeric Alzheimer's amyloid-β peptide inhibits amyloid formation

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Abnormal mitochondrial dynamics, mitochondrial loss and mutant huntingtin oligomers in Huntington's disease: implications for selective neuronal damage

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Brain amyloid-β oligomers in ageing and Alzheimer’s disease

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Calcium Signaling and Amyloid Toxicity in Alzheimer Disease

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Amyloid-β-Induced Pathological Behaviors Are Suppressed byGinkgo bilobaExtract EGb 761 and Ginkgolides in TransgenicCaenorhabditis elegans

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Formation of Toxic Oligomeric α-Synuclein Species in Living Cells

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Are amyloid diseases caused by protein aggregates that mimic bacterial pore-forming toxins?

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The two faces of protein misfolding: gain‐ and loss‐of‐function in neurodegenerative diseases

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Phenolic Compounds Prevent Alzheimer’s Pathology through Different Effects on the Amyloid-β Aggregation Pathway

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A Mouse Model of Amyloid β Oligomers: Their Contribution to Synaptic Alteration, Abnormal Tau Phosphorylation, Glial Activation, and Neuronal Loss In Vivo

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In Vivo Assessment of Brain Interstitial Fluid with Microdialysis Reveals Plaque-Associated Changes in Amyloid-β Metabolism and Half-Life

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Aplysia CPEB Can Form Prion-like Multimers in Sensory Neurons that Contribute to Long-Term Facilitation

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ANS Binding Reveals Common Features of Cytotoxic Amyloid Species

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Monitoring and Inhibition of Insulin Fibrillation by a Small Organic Fluorogen with Aggregation-Induced Emission Characteristics

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Fibril Fragmentation Enhances Amyloid Cytotoxicity

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Protein aggregates in Huntington's disease

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Amyloid-β forms fibrils by nucleated conformational conversion of oligomers

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