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Fig. 5 | Biology Direct

Fig. 5

From: The struggle by Caenorhabditis elegans to maintain proteostasis during aging and disease

Fig. 5

Neuronal Regulation of Protein Misfolding and the Heat Shock Response. a Top: Sensory neurons induce the organismal HSR under conditions of acute thermal stress and block the upregulation of Hsps in non-neuronal tissues under conditions of chronic misfolding but normal temperature. Bottom: Genetic ablation of sensory neurons results in an inability to launch an organismal HSR, but de-repression of Hsp expression results in their upregulation in non-neuronal tissues and concomitant suppression of the aggregation of disease-associated proteins. b Cholinergic signaling at the neuromuscular junction (NMJ). Red dots represent acetylcholine and the acetylcholine receptor (AchR) is indicated. Left: normal conditions; middle: conditions of moderate increase in acetylcholine signaling to upregulation of the AchR; right: extreme increase in acetylcholine signaling due to lack of the inhibitory neurotransmitter GABA. Downstream effects on aggregation and toxicity of disease-associated proteins are indicated. c Schematic graphical representation of the effects of cholinergic signaling on the aggregation of disease associated proteins. The green block represents the narrow window during which acetylcholine signaling is neither too high nor too low to suppress aggregation via the induction of a heat shock response in muscle cells

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