A novel AIFM1 mutation expands the phenotype to an infantile motor neuron disease.
Nazzareno DiodatoGiorgio TascaDaniela VerrigniAdele D'AmicoTeresa RizzaGiulia TozziDiego MartinelliMargherita VerardoFederica InvernizziAlessia NascaEmanuele BellacchioDaniele GhezziFiorella PiemonteCarlo Dionisi-ViciRosalba CarrozzoEnrico BertiniPublished in: European journal of human genetics : EJHG (2015)
AIFM1 is a gene located on the X chromosome, coding for AIF (Apoptosis-Inducing Factor), a mitochondrial flavoprotein involved in caspase-independent cell death. AIFM1 mutations have been associated with different clinical phenotypes: a severe infantile encephalopathy with combined oxidative phosphorylation deficiency and the Cowchock syndrome, an X-linked Charcot-Marie-Tooth disease (CMTX4) with axonal sensorimotor neuropathy, deafness and cognitive impairment. In two male cousins with early-onset mitochondrial encephalopathy and cytochrome c oxidase (COX) deficiency, we identified a novel AIFM1 mutation. Muscle biopsies and electromyography in both patients showed signs of severe denervation. Our patients manifested a phenotype that included signs of both cortical and motor neuron involvement. These observations emphasize the role of AIF in the development and function of neurons.
Keyphrases
- early onset
- cell death
- end stage renal disease
- oxidative stress
- ejection fraction
- late onset
- newly diagnosed
- cognitive impairment
- peritoneal dialysis
- skeletal muscle
- spinal cord injury
- genome wide
- spinal cord
- cell proliferation
- gene expression
- functional connectivity
- drug induced
- transcription factor
- smoking cessation
- optical coherence tomography