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Diana L. Castillo-Carranza

Researcher at University of Texas Medical Branch

Publications -  35
Citations -  3657

Diana L. Castillo-Carranza is an academic researcher from University of Texas Medical Branch. The author has contributed to research in topics: Tau protein & Amyloid. The author has an hindex of 25, co-authored 34 publications receiving 3023 citations. Previous affiliations of Diana L. Castillo-Carranza include University of Monterrey.

Papers
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Journal ArticleDOI

Tau oligomers impair memory and induce synaptic and mitochondrial dysfunction in wild-type mice

Cristian A. Lasagna-Reeves, +5 more
- 06 Jun 2011 - 
TL;DR: It is reported that oligomers of recombinant full-length human tau protein are neurotoxic in vivo after subcortical stereotaxic injection into mice, and suggests that tau oligomers induce neurodegeneration by affecting mitochondrial and synaptic function, both of which are early hallmarks in AD and other tauopathies.
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Identification of oligomers at early stages of tau aggregation in Alzheimer's disease

Cristian A. Lasagna-Reeves, +7 more
- 17 Jan 2012 - 
TL;DR: A novel tau oligomer‐specific antibody is engineered and used to elucidate the temporal course and biochemical features of oligomers during NFT development in AD brain and highlight the suitability of tAU oligomers as therapeutic targets in AD and related tauopathies.
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Alzheimer brain-derived tau oligomers propagate pathology from endogenous tau.

Cristian A. Lasagna-Reeves, +7 more
- 03 Oct 2012 - 
TL;DR: It is observed for the first time that these authentic brain-derived tau oligomers propagate abnormal tau conformation of endogenous murine tau after prolonged incubation.
Journal ArticleDOI

Preparation and Characterization of Neurotoxic Tau Oligomers

Cristian A. Lasagna-Reeves, +4 more
- 08 Nov 2010 - 
TL;DR: It is shown that both Aβ and α-synuclein oligomers induce tau aggregation and the formation of β-sheet-rich neurotoxic tau oligomers.
Journal ArticleDOI

Passive immunization with tau oligomer monoclonal antibody reverses tauopathy phenotypes without affecting hyperphosphorylated neurofibrillary tangles

Diana L. Castillo-Carranza, +10 more
- 19 Mar 2014 - 
TL;DR: A novel tau oligomer-specific monoclonal antibody for passive immunization in mice expressing mutant human tau was sufficient to reverse both locomotor and memory deficits in a mouse model of tauopathy for 60 d and demonstrates that antibody protection is mediated by extracellular and rapid peripheral clearance.