Familial Amyloid Polyneuropathy, Type V

Overview of Familial Amyloid Polyneuropathy, Type V

Most recent studies have shown that Familial Amyloid Polyneuropathy, Type V shares some biological mechanisms with amyloid-deposition, amyloidosis, amyloidosis-familial, avellino-corneal-dystrophy, corneal-diseases, corneal-dystrophy-lattice-type-3, corneal-erosion, cranial-nerve-diseases, dystrophy, granular-corneal-dystrophy, hereditary-corneal-dystrophy, macular-corneal-dystrophy, meretoja-syndrome, plaque-amyloid, primary-systemic-amyloidosis, stromal-corneal-dystrophy.

Among the many pathways, these few ones have gauged particular interests from scientists studying Familial Amyloid Polyneuropathy, Type V, and have been seen in publications frequently: Aging, Angiogenesis, Cell Cycle, Cell-matrix Adhesion, Localization, Pathogenesis, Protein Folding, Wound Healing

Quite a number of genes have been found to play important roles in Familial Amyloid Polyneuropathy, Type V, such as ACD, APCS, APOE, CHST6, CLU, CRP, FANCF, GSN, KRT3, MLYCD, PTK2B, TACSTD2, TEAD1, TGFB1, TGFBI, USP9X. 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.

Familial Amyloid Polyneuropathy, Type V Related Genes

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Pathways Related to Familial Amyloid Polyneuropathy, Type V

This information is being compiled and will come in a future update

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