Patricia Inácio, PhD, science writer —

Patricia holds her PhD in cell biology from the University Nova de Lisboa, Portugal, and has served as an author on several research projects and fellowships, as well as major grant applications for European agencies. She also served as a PhD student research assistant in the Department of Microbiology & Immunology, Columbia University, New York, for which she was awarded a Luso-American Development Foundation (FLAD) fellowship.

Articles by Patricia Inácio

ALS Patients’ Motor Neurons Degenerate at Accelerated Rate With Specific Enzyme

Researchers discovered that a metalloproteinase specialized in the degradation of chondroitin sulfate proteoglycans, called ADAMTS-4, promotes neurodegeneration in a mouse model for human amyotrophic lateral sclerosis (ALS). The study, “ADAMTS-4 promotes neurodegeneration in a mouse model of amyotrophic lateral sclerosis,” was published in the journal Molecular Neurodegeneration. ALS,…

Increased Risk of ALS Appears Linked to Physical Trauma at Early Age

Physical trauma at earlier ages appears associated with an increased risk of amyotrophic lateral sclerosis (ALS), according to a study titled “Physical Trauma and Amyotrophic Lateral Sclerosis: A Population-Based Study Using Danish National Registries” published in the American Journal of Epidemiology. ALS, also known as Lou Gehrig’s disease and Charcot…

Perturbed Transport into Cellular Nucleus Linked to ALS

Three recent studies published in the journals Nature and Nature Neuroscience identified a mutation in some forms of amyotrophic lateral sclerosis (ALS) and frontotemporal degeneration (FTD) that leads to neuronal death by disrupting the movement of molecules within the cellular nucleus. ALS and FTD are characterized by death…

Two New Studies Identify Disrupted Trafficking Inside Neurons as the Cause for Known ALS Mutation

Two new studies, one entitled “GGGGCC repeat expansion in C9orf72 compromises nucleocytoplasmic transport” and another “The C9orf72 repeat expansion disrupts nucleocytoplasmic transport”, report the discovery of a key mechanism underlying amyotrophic lateral sclerosis’ onset which is associated with C9orf72 mutation (the most common genetic defect…

ALS P56S-VAPB Mutation Suppresses Muscle Fiber Formation

In a recent study entitled “ALS-Linked P56S-VAPB Mutation Impairs the Formation of Multinuclear Myotube in C2C12 Cells” researchers investigated the role of a mutation associated with ALS type-8 (ALS8)  – P56S-VAPB mutation – on skeletal muscle cells homeostasis and muscle formation. The study was published in the…