nosogenesis

nos·o·gen·e·sis

, nosogeny (nos'ō-jen'ĕ-sis, no-soj'ĕ-nē),
Rarely used terms for pathogenesis.
[noso- + G. genesis, production]
References in periodicals archive ?
Results: There are many amounts of data supporting the view that AD pathogenesis so far there mainly are A[sz] toxicity, tau protein, gene mutation, synaptic damages, intermediate neurons and network abnormalities, changes in mitochondrial function, chemokines, etc., Its nosogenesis may be involved in multiple theories and involved in multiple molecular signaling pathways, including A[sz], tau protein, and synaptic anomaly; mutual relationship between the mechanisms urge jointly neuronal degeneration.
At present, there are mainly beta-amyloid (A[sz]) theory, tau protein theory, nerve, and blood vessel theory are some of these in the aspect of the interpretation to the nosogenesis of AD.
Researches in recent years have shown that microRNA (miRNA) was closely related to the nosogenesis of AD, miRNA playing an important role in AD and gene translation expression.[6] The study by Li et al .[7] have found that ApoE4 gene appears frequently in the cases of the advanced AD patients and that ApoE4 is the risk factor of AD occurrence, the frequent occurrence rate of ApoE4 gene positively related to the probability of AD.
Tau protein may be able to diffuse from a brain cell to another brain cell, suggesting that the diffusion of tau among cells is prevented passed could by the antibody of blocking tau protein.[17] In the model of tau-P301L transgenic mouse, immunization therapy can facilitate the defense reaction of microglial cell, accelerate the clearing to tau protein, and protect nerve cell from the toxic effect induced by tau.[18] Research [19] challenges the neurotoxic effects of tau phosphorylation in AD nosogenesis and the research found that at least in the early stage of AD, phosphorylation of characteristic sites in tau protein was able to inhibit the toxicity of A[sz], being that tau phosphorylation-mediated by p38MAPK can antagonize the postsynaptic excitation toxicity caused by A[sz].
Therefore, research on nosogenesis and therapies to prevent and treat pediatric NAFLD is absolutely necessary.
This demonstrated that the balance of wild and mutant-type huntingtin may be a momentous regulator of nosogenesis in HD.
Primary Meige's syndrome's nosogenesis is unclear; while secondary Meige's syndrome could be related to the upper brain stem and abnormal basal ganglia dopamine receptor hypersensitivity, the hyperactive cholinergic nervous system (e.g., basal ganglia), low Gamma-aminobutyric Acid (GABA) function.
Its possible nosogenesis is the hypersensitivity of the basal ganglia dopamine receptor.