Tau deletion impairs intracellular β-amyloid-42 clearance and leads to more extracellular plaque deposition in gene transfer models

Molecular neurodegeneration

Volumn 9, Issue , 2014, Pages 46-

  Lonskaya, Irina ^a   Hebron, Michaeline ^a   Chen, Wenqiang ^a   Schachter, Joel ^a   Moussa, Charbel ^b  

^a Georgetown University Medical Center ^*

^b GEORGETOWN UNIVERSITY MEDICAL CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

AMYLOID BETA PROTEIN; AMYLOID BETA-PROTEIN (1-42); PEPTIDE FRAGMENT; PROTEASOME; TAU PROTEIN;

ALZHEIMER DISEASE; AMYLOID PLAQUE; ANIMAL; AUTOPHAGY; C57BL MOUSE; DISEASE MODEL; ENZYME LINKED IMMUNOSORBENT ASSAY; EXTRACELLULAR SPACE; HUMAN; IMMUNOHISTOCHEMISTRY; KNOCKOUT MOUSE; MALE; METABOLISM; MOUSE; PATHOLOGY; PHOSPHORYLATION; WESTERN BLOTTING;

ALZHEIMER DISEASE; AMYLOID BETA-PEPTIDES; ANIMALS; AUTOPHAGY; BLOTTING, WESTERN; DISEASE MODELS, ANIMAL; ENZYME-LINKED IMMUNOSORBENT ASSAY; EXTRACELLULAR SPACE; HUMANS; IMMUNOHISTOCHEMISTRY; MALE; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; PEPTIDE FRAGMENTS; PHOSPHORYLATION; PLAQUE, AMYLOID; PROTEASOME ENDOPEPTIDASE COMPLEX; TAU PROTEINS;

EID: 84964312590     PISSN: None     EISSN: 17501326     Source Type: Journal    
DOI: 10.1186/1750-1326-9-46     Document Type: Article

References (0)