Neuronal regulation of immunity: why, how and where?

Schiller, Maya; Ben-Shaanan, Tamar L.; Rolls, Asya

doi:10.1038/s41577-020-0387-1

Cited by 149 publications

(124 citation statements)

References 273 publications

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“…The specific pathway through which rtfMRI-nf-induced modulation of central KP metabolism putatively alters peripheral KP metabolism is unclear since comparatively little is known about how the brain regulates the immune system. What is known is that the hypothalamic–pituitaryadrenal (HPA) axis regulates immunity via the secretion of hormones, the para/sympathetic nervous system alters immunity via “hard-wired” connections between the vagus and other sensory nerves and the lymph nodes, and the meningeal lymphatic system delivers immune cells and immune-related signals to the periphery ( Schiller et al, 2020 ). Conceivably, a rtfMRI-nf-mediated restoration of hippocampal-amygdalar function has “top-down” effects on peripheral immunity via one or more of these pathways.…”

Section: Discussionmentioning

confidence: 99%

Real-time fMRI neurofeedback amygdala training may influence kynurenine pathway metabolism in major depressive disorder

Tsuchiyagaito

Smith

El-Sabbagh

et al. 2021

NeuroImage: Clinical

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Highlights rtfMRI-nf LA emotional training reduces depressive symptoms. rtfMRI-nf LA training increases KynA/3-HK, a neuroprotective index. Baseline KynA/QA is associated with the ability to upregulate the LA. In partial responder group LA upregulation positively correlates with KynA/QA. In partial responder group LA upregulation inversely correlates with MADRS. Modulation of the KP may drive rtfMRI-nf-induced changes in neuroplasticity. Non-specific effects cannot be ruled out due to the lack of a sham control.

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Section: Discussionmentioning

confidence: 99%

Real-time fMRI neurofeedback amygdala training may influence kynurenine pathway metabolism in major depressive disorder

Tsuchiyagaito

Smith

El-Sabbagh

et al. 2021

NeuroImage: Clinical

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“…In conclusion, we hope that our reflections may offer an additional contribution for further discussion on the origin, pathological mechanism, and possible evolution of peripheral vascular alterations in eating disorders and to their better diagnosis, prevention, and treatment. There is a bidirectional relationship between autoimmunity and anorexia nervosa: autoimmune diseases and eating disorders give each other a mutual increased risk [42,43].…”

Section: Discussionmentioning

confidence: 99%

Peripheral Vascular Abnormalities in Anorexia Nervosa: A Psycho-Neuro-Immune-Metabolic Connection

Sirufo

Ginaldi

Martinis

2021

IJMS

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Immune, neuroendocrine, and autonomic nervous system dysregulation in anorexia nervosa lead to cardiovascular complications that can potentially result in increased morbidity and mortality. It is suggested that a complex non-invasive assessment of cardiovascular autonomic regulation—cardiac vagal control, sympathetic vascular activity, and cardiovascular reflex control—could represent a promising tool for early diagnosis, personalized therapy, and monitoring of therapeutic interventions in anorexia nervosa particularly at a vulnerable adolescent age. In this view, we recommend to consider in the diagnostic route, at least in the subset of patients with peripheral microvascular symptoms, a nailfold video-capillaroscopy as an easy not invasive tool for the early assessing of possible cardiovascular involvement.

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“…Despite glial cells having been reported to induce deregulation in mitochondria and endoplasmic reticulum dysfunction resulting in bioenergetic and Ca 2+ homeostasis disruption [ 99 ], neuroinflammation is critical for AD since it appears to modulate the disease progression [ 100 , 101 ]. The integration of the immune system and the central nervous system was recently reviewed [ 102 ]. In AD, the neuroinflammation relies on innate immune responses mediated by microglia [ 103 ].…”

Section: General Aspects Of Mitogen-activated Protein Kinases (Mapmentioning

confidence: 99%

c-Jun N-Terminal Kinase Inhibitors as Potential Leads for New Therapeutics for Alzheimer’s Diseases

Rehfeldt

Majolo

Goettert

et al. 2020

IJMS

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Alzheimer’s Disease (AD) is becoming more prevalent as the population lives longer. For individuals over 60 years of age, the prevalence of AD is estimated at 40.19% across the world. Regarding the cognitive decline caused by the disease, mitogen-activated protein kinases (MAPK) pathways such as the c-Jun N-terminal kinase (JNK) pathway are involved in the progressive loss of neurons and synapses, brain atrophy, and augmentation of the brain ventricles, being activated by synaptic dysfunction, oxidative stress, and excitotoxicity. Nowadays, AD symptoms are manageable, but the disease itself remains incurable, thus the inhibition of JNK3 has been explored as a possible therapeutic target, considering that JNK is best known for its involvement in propagating pro-apoptotic signals. This review aims to present biological aspects of JNK, focusing on JNK3 and how it relates to AD. It was also explored the recent development of inhibitors that could be used in AD treatment since several drugs/compounds in phase III clinical trials failed. General aspects of the MAPK family, therapeutic targets, and experimental treatment in models are described and discussed throughout this review.

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Neuronal regulation of immunity: why, how and where?

Cited by 149 publications

References 273 publications

Real-time fMRI neurofeedback amygdala training may influence kynurenine pathway metabolism in major depressive disorder

Real-time fMRI neurofeedback amygdala training may influence kynurenine pathway metabolism in major depressive disorder

Peripheral Vascular Abnormalities in Anorexia Nervosa: A Psycho-Neuro-Immune-Metabolic Connection

c-Jun N-Terminal Kinase Inhibitors as Potential Leads for New Therapeutics for Alzheimer’s Diseases

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