The present study was designed to determine the effects of peripheral inflammation, using tooth pulp inflammation as a model, on regulation of BDNF expression in TG neurons of juvenile rats and mice.
Although MSCs can be isolated from almost all tissues, including liver, lung, fetal pancreas, trabecular bone, synovium, skeletal muscle, deciduous teeth, and peripheral blood, the byproducts of birth, such as placenta, amniotic membrane, umbilical cord (UC), and umbilical cord blood (UCB) [ 5– 12], are the most promising sources in terms of youthfulness [ 4].
Missense mutants in the late endosomal Rab7 GTPase cause the autosomal dominant peripheral neuropathy Charcot-Marie-Tooth disease type 2B (CMT2B).
Mutations in GDAP1 lead to the peripheral neuropathy Charcot-Marie-Tooth disease (CMT), affecting both Schwann cells, the myelinating glia of the peripheral nervous system, and neurons [2].
Growing evidences suggest that GAN is a continuum with the peripheral neuropathy Charcot-Marie-Tooth diseases type 2 (CMT2).
The most common genetic cause of the inherited peripheral neuropathy Charcot-Marie-Tooth disease is the PMP22 duplication; otherwise, CNVs have been considered rare.
Stimuli on the peripheral surfaces of the tooth, e.g. heat from grinding processes, induce the production of secondary or reparative (tertiary) dentine by odontoblasts.
Mutations in either active or inactive members of this family bring about human disease, which involves chiefly skeletal muscle (X-linked myotubular myopathy [XLMTM]) or peripheral neurons (Charcot-Marie-Tooth [CMT] neuropathies) [ 2- 4].
Of these, Ndrg1 was considered as an especially good candidate since mutations in the human orthologue have been shown to be the cause of a demyelinating peripheral neuropathy, Charcot-Marie-Tooth disease type 4D.
Of note, mutations in Mfn2 cause the autosomal dominant peripheral neuropathy, Charcot Marie-Tooth disease 2A, while reduced expression of the protein has been found in diabetic and obese patients.
