Long-term electromagnetic field treatment enhances brain mitochondrial function of both Alzheimer's transgenic mice and normal mice: A mechanism for electromagnetic field-induced cognitive benefit?

Neuroscience

Volumn 185, Issue , 2011, Pages 135-149

  Dragicevic, N ^a   Bradshaw, P C ^a   Mamcarz, M ^a   Lin, X ^b   Wang, L ^a   Cao, C ^b,c   Arendash, G W ^a,d  

^a UNIVERSITY OF SOUTH FLORIDA   (United States)

^b UNIVERSITY OF SOUTH FLORIDA   (United States)

^c UNIVERSITY OF SOUTH FLORIDA   (United States)

^d UNIVERSITY OF SOUTH FLORIDA   (United States)

Author keywords

Alzheimer's; Electromagnetic fields; Mitochondrial function; Transgenic mice

Indexed keywords

ADENOSINE TRIPHOSPHATE; AMYLOID BETA PROTEIN; OLIGOMER; REACTIVE OXYGEN METABOLITE;

AGED; ALZHEIMER DISEASE; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BRAIN CORTEX; BRAIN MITOCHONDRION; BRAIN TEMPERATURE; COGNITION; CONTROLLED STUDY; DISORDERS OF MITOCHONDRIAL FUNCTIONS; ELECTROMAGNETIC FIELD; HIPPOCAMPUS; MITOCHONDRIAL MEMBRANE POTENTIAL; MITOCHONDRIAL RESPIRATION; MOUSE; NONHUMAN; PRIORITY JOURNAL; TRANSGENIC MOUSE;

ADENOSINE TRIPHOSPHATE; ALZHEIMER DISEASE; AMYLOID BETA-PEPTIDES; AMYLOID BETA-PROTEIN PRECURSOR; ANALYSIS OF VARIANCE; ANIMALS; BODY TEMPERATURE; BRAIN; DISEASE MODELS, ANIMAL; ELECTRON TRANSPORT COMPLEX IV; ENZYME-LINKED IMMUNOSORBENT ASSAY; HUMANS; MAGNETIC FIELD THERAPY; MEMBRANE POTENTIAL, MITOCHONDRIAL; MICE; MICE, TRANSGENIC; MITOCHONDRIA; MUTATION; PEPTIDE FRAGMENTS; PRESENILIN-1; REACTIVE OXYGEN SPECIES;

EID: 79956272790     PISSN: 03064522     EISSN: 18737544     Source Type: Journal    
DOI: 10.1016/j.neuroscience.2011.04.012     Document Type: Article

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