Disease Info Card

Hallervorden-spatz Syndrome

Information about Hallervorden-spatz Syndrome: characteristics, related genes and pathways, plus antibodies you can use for research. This page is being enriched constantly, if you see some information you would like this page to include please send your suggestions to us.

Overview of Hallervorden-spatz Syndrome

Most recent studies have shown that Hallervorden-spatz Syndrome shares some biological mechanisms with abnormal-degeneration, ataxia, atrophy, basal-ganglia-diseases, brain-diseases, dementia, dysarthria, dystonia-disorders, dystrophy, globus-hystericus, huntington-disease, infantile-neuroaxonal-dystrophy, movement-disorders, nerve-degeneration, nervousness, neuroaxonal-dystrophies, neurodegenerative-disorders, parkinson-disease, retinitis-pigmentosa, secondary-parkinson-disease.

Among the many pathways, these few ones have gauged particular interests from scientists studying Hallervorden-spatz Syndrome, and have been seen in publications frequently: Aging, Bile Acid Conjugation, Cellular Localization, Cognition, Conjugation, Ion Transport, Lipid Homeostasis, Localization, Macrophage Activation, Myelination, Neuroprotection, Pathogenesis, Pigment Accumulation, Pigmentation, Protein Oxidation, Proteolysis, Reflex, Response To Stimulus, Transport

Quite a number of genes have been found to play important roles in Hallervorden-spatz Syndrome, such as ACAT1, CHST3, CP, FXN, GFER, GJA1, LRP2, MAPT, MCF2L, PANK1, PANK2, PLA2G6, RNF130, SCG2, SGSH, SIGLEC1, SNCA, SPAG9, TNC. See what Boster has to offer for the research of these genes by clicking the gene name links below and view a more detailed info card/product listing for that gene.

In a later update, we will include information such as current drugs and therapy solutions as well as on-going and past clinical trials for this disease. Plesae stay updated.