Lack of exon 10 in the murine tau gene results in mild sensorimotor defects with aging

BMC Neuroscience

Volumn 14, Issue , 2013, Pages

  Gumucio, Astrid ^a   Lannfelt, Lars ^a   Nilsson, Lars N G ^a,b  

^a UPPSALA UNIVERSITY   (Sweden)

^b OSLO UNIVERSITY HOSPITAL   (Norway)

Author keywords

Alternative splicing; Alzheimer's disease; Knockout mice; Microtubule; Tau

Indexed keywords

TAU PROTEIN;

ABLATION THERAPY; AGING; ALLELE; ALTERNATIVE RNA SPLICING; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ANXIETY; ARTICLE; CONTROLLED STUDY; EXON; FEMALE; GENE DELETION; GENE TARGETING; GRIP STRENGTH; LEARNING; MALE; MICROTUBULE; MORPHOLOGY; MOUSE; MUSCLE STRENGTH; NONHUMAN; PHENOTYPE; PROTEIN SYNTHESIS; SENSORIMOTOR FUNCTION; SENSORIMOTOR NEUROPATHY; STATE DEPENDENT LEARNING; WILD TYPE;

AGING; ALTERNATIVE SPLICING; ANIMALS; BEHAVIOR, ANIMAL; BLOTTING, WESTERN; BRAIN; EXONS; MICE; MICE, KNOCKOUT; MUSCLE STRENGTH; POLYMERASE CHAIN REACTION; PSYCHOMOTOR PERFORMANCE; TAU PROTEINS;

EID: 84887973955     PISSN: None     EISSN: 14712202     Source Type: Journal    
DOI: 10.1186/1471-2202-14-148     Document Type: Article

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