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Tau Oligomers: The Toxic Player at Synapses in Alzheimer's DiseaseCerebral Microvascular Accumulation of Tau Oligomers in Alzheimer's Disease and Related Tauopathies.The formation of tau pore-like structures is prevalent and cell specific: possible implications for the disease phenotypes.Tau oligomers impair memory and induce synaptic and mitochondrial dysfunction in wild-type mice.Rapid accumulation of endogenous tau oligomers in a rat model of traumatic brain injury: possible link between traumatic brain injury and sporadic tauopathiesTau Oligomers: Cytotoxicity, Propagation, and Mitochondrial Damage.Tau oligomers as potential targets for immunotherapy for Alzheimer's disease and tauopathies.Therapeutic approaches against common structural features of toxic oligomers shared by multiple amyloidogenic proteins.Advances in therapeutics for neurodegenerative tauopathies: moving toward the specific targeting of the most toxic tau species.Amyloid-β oligomers as a template for secondary amyloidosis in Alzheimer's disease.Dual role of p53 amyloid formation in cancer; loss of function and gain of toxicity.Formation of immunoglobulin light chain amyloid oligomers in primary cutaneous nodular amyloidosis.Pitx3 promoter directs Cre-recombinase specifically in a human neuroblastoma cell line.Alzheimer brain-derived tau oligomers propagate pathology from endogenous tauTau Oligomers Associate with Inflammation in the Brain and Retina of Tauopathy Mice and in Neurodegenerative Diseases.Design of metastable β-sheet oligomers from natively unstructured peptide.Antibody against Small Aggregated Peptide Specifically Recognizes Toxic Aβ-42 Oligomers in Alzheimer's Disease.Pathological interface between oligomeric alpha-synuclein and tau in synucleinopathies.Specific targeting of tau oligomers in Htau mice prevents cognitive impairment and tau toxicity following injection with brain-derived tau oligomeric seeds.Tau immunotherapy modulates both pathological tau and upstream amyloid pathology in an Alzheimer's disease mouse model.Tau Oligomers Derived from Traumatic Brain Injury Cause Cognitive Impairment and Accelerate Onset of Pathology in Htau Mice.Passive immunization with Tau oligomer monoclonal antibody reverses tauopathy phenotypes without affecting hyperphosphorylated neurofibrillary tangles.α-Synuclein Oligomers Induce a Unique Toxic Tau Strain.
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description
hulumtuese
@sq
researcher
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wetenschapper
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հետազոտող
@hy
name
Diana L Castillo-Carranza
@ast
Diana L Castillo-Carranza
@en
Diana L Castillo-Carranza
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Diana L Castillo-Carranza
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type
label
Diana L Castillo-Carranza
@ast
Diana L Castillo-Carranza
@en
Diana L Castillo-Carranza
@es
Diana L Castillo-Carranza
@nl
altLabel
Diana Castillo-Carranza
@en
prefLabel
Diana L Castillo-Carranza
@ast
Diana L Castillo-Carranza
@en
Diana L Castillo-Carranza
@es
Diana L Castillo-Carranza
@nl
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56013636500
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0000-0003-2511-949X