Alexandro Gianforcaro

Learn More
Vitamin D has been demonstrated to influence multiple aspects of amyotrophic lateral sclerosis (ALS) pathology. Both human and rodent central nervous systems express the vitamin D receptor (VDR) and/or its enzymatic machinery needed to fully activate the hormone. Clinical research suggests that vitamin D treatment can improve compromised human muscular(More)
BACKGROUND We previously demonstrated that dietary vitamin D(3) at 10x the adequate intake (AI) attenuates the decline in functional capacity in the G93A mouse model of ALS. We hypothesized that higher doses would elicit more robust changes in functional and disease outcomes. OBJECTIVE To determine the effects of dietary vitamin D(3) at 50xAI on(More)
BACKGROUND Vitamin D has antioxidant, anti-inflammatory, and neuroprotective properties, and may mitigate amyotrophic lateral sclerosis (ALS) pathology. AIMS To determine the effects of dietary vitamin D(3) (D(3)) at 10-fold the adequate intake (AI) on functional and disease outcomes and lifespan in the transgenic G93A mouse model of ALS. METHODS(More)
UNLABELLED Amyotrophic lateral sclerosis (ALS) is a neuromuscular disease characterized by motor neuron death in the central nervous system. Vitamin D supplementation increases antioxidant activity, reduces inflammation and improves motor neuron survival. We have previously demonstrated that vitamin D(3) supplementation at 10× the adequate intake improves(More)
BACKGROUND Dietary vitamin D3 (D3) restriction reduces paw grip endurance and motor performance in G93A mice, and increases inflammation and apoptosis in the quadríceps of females. ALS, a neuromuscular disease, causes progressive degeneration of motor neurons in the brain and spinal cord. OBJECTIVE We analyzed the spinal cords of G93A mice following(More)
  • 1