Produced by the bodys cells while we are fighting an infection that are powerfully sleep-inducing.

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Open access

Abstract

Alpha-synuclein (α-syn) has been suggested to have many functions including, vesicle transport in neurons, transcriptional regulator, modulator of immune cell maturation and response, and a role as an antimicrobial peptide. This protein forms insoluble aggregates, called Lewy bodies, in several neurodegenerative diseases, termed synucleinopathies, including Parkinson's disease (PD), Multiple System Atrophy, and Lewy Body Dementia, and aggregates are also commonly found in Alzheimer's disease. Moreover, multiplications and point mutations in the gene cause rare autosomal dominant forms of parkinsonism, which resemble sporadic PD. It has been suggested that the accumulation of α-syn in the monomeric state followed by aggregation of the protein and seeding of further pathogenic α-syn aggregates are key steps in the pathogenesis of synucleinopathies. The triggers of α-syn aggregation in neurodegeneration are unknown, but inflammation caused by bacterial and viral pathogens or exposure to environmental toxins have been implicated.

The purpose of this review is to present emerging evidence that α-syn may play a role in the immune response to pathogens. We present recent findings suggesting that upregulation of α-syn levels is a normal response to infections. We propose that under certain conditions (e.g., dysregulated inflammatory responses due to genetic predisposition and aging), monomeric α-syn will form oligomers that are taken up by nerve endings and undergo axonal transport to the central nervous system, where they can aggregate into pathogenic fibrils. Under unfavorable conditions, we suggest that this process can trigger neurodegenerative disease. Therefore, a deeper understanding of the roles of α-syn in the immune system could provide crucial insights into the origins of synucleinopathies.

Keywords

Parkinson's disease

Multiple System Atrophy

Synucleinopathy

Viral infections

Infection

© 2022 The Authors. Published by Elsevier Inc.

Review articlePhysiological feelings☆

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Open access

Highlights

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Peripheral physiological changes can be perceived as feelings via interoception.

Both perceived and unperceived interoceptive information contribute to emotions.

The forebrain can generate physiological feelings without actual peripheral events.

Interacting networks of afferent and efferent signals generate physiological feelings.

Physiological feelings contribute to survival, reproduction and emotion regulation.

Abstract

The role of peripheral physiology in the experience of emotion has been debated since the 19th century following the seminal proposal by William James that somatic responses to stimuli determine subjective emotion. Subsequent views have integrated the forebrain's ability to initiate, represent and simulate such physiological events. Modern affective neuroscience envisions an interacting network of “bottom-up” and “top-down” signaling in which the peripheral (PNS) and central nervous systems both receive and generate the experience of emotion. “Feelings” serves as a term for the perception of these physical changes whether emanating from actual somatic events or from the brain's representation of such. “Interoception” has come to represent the brain's receipt and representation of these actual and “virtual” somatic changes that may or may not enter conscious awareness but, nonetheless, influence feelings. Such information can originate from diverse sources including endocrine, immune and gastrointestinal systems as well as the PNS. We here examine physiological feelings from diverse perspectives including current and historical theories, evolution, neuroanatomy and physiology, development, regulatory processes, pathology and linguistics.

Keywords

Emotion

Feelings

Interoception

Somatic markers

Emotion regulation

Autonomic nervous system

Insula

© 2019 The Authors. Published by Elsevier Ltd.