Towards Alzheimer's root cause: ECSIT as an integrating hub between oxidative stress, inflammation and mitochondrial dysfunction: Hypothetical role of the adapter protein ECSIT in familial and sporadic Alzheimer's disease pathogenesis

BioEssays

Volumn 34, Issue 7, 2012, Pages 532-541

  Soler López, Montserrat ^a   Badiola, Nahuai ^a   Zanzoni, Andreas ^a   Aloy, Patrick ^a,b  

^a INSTITUTE FOR RESEARCH IN BIOMEDICINE   (Spain)

^b INSTITUCIÓ CATALANA DE RECERCA I ESTUDIS AVANÇATS ICREA   (Spain)

Author keywords

Alzheimer's disease; ECSIT; Inflammation; Network biology; Oxidative stress

Indexed keywords

AMYLOID BETA PROTEIN; EVOLUTIONARILY CONSERVED SIGNALLING INTERMEDIATE IN TOLL PATHWAY PROTEIN; PROTEIN; UNCLASSIFIED DRUG;

ALZHEIMER DISEASE; APOPTOSIS; ARTICLE; CELL DAMAGE; CELL DEATH; DISEASE PREDISPOSITION; DISORDERS OF MITOCHONDRIAL FUNCTIONS; HOMEOSTASIS; HUMAN; IMMUNE RESPONSE; IMMUNE SYSTEM; MITOCHONDRION; NERVOUS SYSTEM INFLAMMATION; NEUROPROTECTION; NONHUMAN; OXIDATIVE STRESS; PATHOGENESIS; PROTEIN ANALYSIS; PROTEIN INTERACTION; SIGNAL TRANSDUCTION; SYNAPSE;

ADAPTOR PROTEINS, SIGNAL TRANSDUCING; AGE OF ONSET; ALZHEIMER DISEASE; AMYLOID BETA-PEPTIDES; APOPTOSIS; CHROMOSOMES, HUMAN; GENETIC PREDISPOSITION TO DISEASE; HOMEOSTASIS; HUMANS; IMMUNITY, INNATE; INFLAMMATION; MITOCHONDRIA; OXIDATIVE STRESS; PRESENILIN-1; PRESENILIN-2; PROTEIN INTERACTION MAPPING; PROTEIN INTERACTION MAPS; SIGNAL TRANSDUCTION;

EID: 84862323532     PISSN: 02659247     EISSN: 15211878     Source Type: Journal    
DOI: 10.1002/bies.201100193     Document Type: Article

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