Intracellular β-amyloid accumulation leads to age-dependent progression of Ca2+ dysregulation in skeletal muscle

Muscle and Nerve

Volumn 42, Issue 5, 2010, Pages 731-738

  Lopez, Josè R ^a   Shtifman, Alexander ^b  

^a BRIGHAM AND WOMEN S HOSPITAL   (United States)

^b TUFTS UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

amyloid; Amyloid precursor protein; Calcium; Calcium influx; Inclusion body myositis; L type Ca2+ channels; Muscle; Ryanodine receptors

Indexed keywords

AMYLOID BETA PROTEIN; CALCIUM; CALCIUM CHANNEL; NIFEDIPINE;

AGING; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CALCIUM HOMEOSTASIS; CALCIUM TRANSPORT; CELL INCLUSION; CELL MEMBRANE DEPOLARIZATION; CONTROLLED STUDY; INCLUSION BODY MYOSITIS; INFLAMMATION; MOUSE; MUSCLE ATROPHY; MUSCLE WEAKNESS; NONHUMAN; PATHOGENESIS; PATHOPHYSIOLOGY; PRIORITY JOURNAL; SARCOPLASMIC RETICULUM; SKELETAL MUSCLE; TRANSGENIC MOUSE;

AGING; AMYLOID BETA-PEPTIDES; AMYLOID BETA-PROTEIN PRECURSOR; ANIMALS; CALCIUM; CALCIUM CHANNELS, L-TYPE; CYTOPLASM; DISEASE PROGRESSION; ELECTRIC STIMULATION; HOMEOSTASIS; HUMANS; MANGANESE COMPOUNDS; MEMBRANE POTENTIALS; MICE; MICE, TRANSGENIC; MICROELECTRODES; MUSCLE FIBERS, SKELETAL; MUSCLE, SKELETAL; MYOSITIS, INCLUSION BODY; PERMEABILITY; SARCOPLASMIC RETICULUM;

EID: 78149300132     PISSN: 0148639X     EISSN: 10974598     Source Type: Journal    
DOI: 10.1002/mus.21745     Document Type: Article

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