path(MESH:Paralysis)

Entity

Name

Paralysis

Namespace

MeSH

Namespace Version

20181007

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/01c9daa61012b37dd0a1bc962521ba51a15b38f1/external/mesh-names.belns

Importantly, approximately 70% of the mice in the placebo group developed hind-limb weakness or paralysis compared to only 20% in the anatabine treatment group (Fig. 1C) showing that the mice treated with anatabine displayed significantly milder disease symptoms than the placebo group PubMed:23383175

The axonal damage in EAE mice leads to well defined clinical signs such as tail paralysis, hind-limb weakness and paralysis PubMed:23383175

There are different forms of amyotrophic lateral sclerosis (ALS), all primarily display widespread death of brainstem and spinal motoneurons, corticospinal degeneration, paralysis of skeletal muscle, and eventual neuronal cell death PubMed:14556719

In addition, a non-functional PSA mutant exacerbated tau pathology in a Drosophila model of tauopathy, while overexpressing PSA ameliorated the tau phenotype and diminished tau levels (10). Overexpressing PSA had a similar effect in the TAUP301L mice, reducing the pathologic phenotype (delaying paralysis, increasing motor neuron density in the spinal cord, decreasing gliosis) and decreasing tau levels (12). PubMed:24027553

During the time course of the treatment (40 days), 25% of Tg Tau P301S placebo mice became paralyzed (3 out of 12) whereas none (0 out of 11) in the anatabine treatment group developed paralysis during the study duration (Figure 1) DOI:10.4172/2168-975X.1000126

For example, the first transgenic C. elegans human disease model was based on the expression of the AD-associated Ab peptide in body wall muscles, resulting in paralysis that could be suppressed by coexpression of transthyretin (29). PubMed:29191965

As a result, the proaggregant lines showed a range of defects including paralysis, axonal degeneration of GABAergic and cholinergic motor neurons, presynaptic defects, synapse loss, and mitochondrial transport defects early in adulthood PubMed:29191965

Although the wild-type tau lines showed a mild late-onset dose-dependent Unc phenotype, TauA152T worms showed early-onset paralysis and acute neuronal dysfunction. PubMed:29191965