Abstract
The heat shock response involved in protein misfolding is linked to the formation of toxic immunogenic proteins with heat shock proteins (HSP) as regulators of amyloid beta aggregation. The defective amyloid beta trafficking between different intracellular compartments is now relevant to HSPs and autoimmunity. Overnutrition, temperature dysregulation, and stress repress the heat shock gene Sirtuin 1 with the induction of HSP regulated amyloid beta aggregation involved in the autoimmune response. Defective circadian rhythm alterations are connected to inactivation of the peripheral sink amyloid beta clearance pathway and related to insulin resistance, protein aggregation, and autoimmune disease in non-alcoholic fatty liver disease (NAFLD) and various neurodegenerative diseases such as Alzheimer’s disease. Nutritional therapy is critical to prevent immunosenescence, and plasma Sirtuin 1 levels should be determined to reverse, stabilize, and prevent protein aggregation with relevance to mitochondrial apoptosis and programmed cell death in chronic diseases.
Highlights
The heat shock response involved in protein misfolding is linked to the formation of toxic immunogenic proteins with heat shock proteins (HSP) as regulators of amyloid beta aggregation
In the developing world elevated LPS are associated with Sirtuin 1 (Sirt 1) dysregulation [19] with autoimmune disease associated with mitochondrial apoptosis, insulin resistance linked to various chronic diseases
Temperature dysregulation and unhealthy diets will corrupt peripheral amyloid clearance pathway linked to immunogenic mediated amyloid beta aggregation relevant beta clearance pathway linked to immunogenic HSP mediated amyloid beta aggregation relevant to to mitophagy, apoptosis autoimmune disease in global chronic disease
Summary
The heat shock response involved in protein misfolding is linked to the formation of toxic immunogenic proteins with heat shock proteins (HSP) as regulators of amyloid beta aggregation. 1 and relevance to autoimmune disease maymay involve the the dysregulation of of immunogenic Under immunogenic HSPs and amyloid beta oligomers associated with cell apoptosis (Figure 1).
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