Vagal Nerve

$9M Grant Funds Study of Gut-Brain Connection in Parkinson’s Disease

A-Synuclein, Gut Dysbiosis, Gut-Brain axis, Symptoms / Diagnosis, Vagal Nerve /

Dr. Michael Kaplitt, a professor of neurological surgery at Weill Cornell Medicine and a longtime leader in developing cutting-edge surgical therapies for movement disorders, leads a team that has been awarded a three-year, $8.9 million grant from the Aligning Science Across Parkinson’s (ASAP) initiative. The grant will fund an ambitious and innovative multi-institutional collaborative effort to study […]

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What Substance P might tell us about the Prognosis and Mechanism of Parkinson’s Disease?

A-Synuclein, Gut-Brain axis, Olfactory, Parkinson's Disease, Vagal Nerve /

The neuropeptide substance P (SP) plays an important role in neurodegenerative disorders, among which Parkinson’s disease (PD). In the present work we have reviewed the involvement of SP and its preferred receptor (NK1-R) in motor and non-motor PD symptoms, in both PD animal models and patients. Despite PD is primarily a motor disorder, non-motor abnormalities,

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A New Kind of Pathogen – The prion-like pathology of amyloid fibrils in Parkinson’s disease

A-Synuclein, Dementia - Lewy Bodies, Gut-Brain axis, Olfactory, Parkinson's Disease, Pre-PD, Vagal Nerve /

This chapter contrasts the prion-like behavior of alphasynuclein in Parkinson’s disease with other prion diseases.In prion diseases, the infectious, amyloid form of theprotein induces the corresponding normally folded proteinto assume the toxic fold, spreading the disease and slowlydestroying the brains of infected patients. Lewy pathologyin Parkinson’s disease appears to spread in a mannersimilar to that

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Clinical and Pre-Clinical Evidence for Enteric α-Synuclein Involvement in Parkinson’s Disease

A-Synuclein, Gut Dysbiosis, Gut Permeability / Leaky Gut, Vagal Nerve /

While commonly attributed to neuronal death in SNpc, postmortem studies have shown α-syn immunoreactivity and LB pathology inthe peripheral, central, and enteric nervous system (ENS).While the etiology of misfolded α-syn is unknown, variousgut microbiota and substrates are associated with α-syndysfunction. Gastrointestinal (GI) dysfunction, a commonfeature in the prodromal phase of PD patients, and histological evidence

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Serum and Fecal Markers of Intestinal Inflammation and Intestinal Barrier Permeability Are Elevated in Parkinson’s Disease

A-Synuclein, Fecal Transplants (FMT), Gut Dysbiosis, Olfactory, Vagal Nerve, Zonulin /

Parkinson’s disease (PD) is characterized by alpha-synuclein misfolding with subsequent intraneuronal amyloid formation and accumulation, low grade neuroinflammatory changes, and selective neurodegeneration. Available evidence suggests that thepathology usually begins in the gut and olfactory mucosa, spreading to the brain via the vagus and olfactory nerves, by a prion-like mechanism. A causal relationship has not been

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The gut-brain connection in the pathogenicity of Parkinson disease: Putative role of autophagy

Autophagy, Gut Dysbiosis, Gut-Brain axis, Vagal Nerve /

Hence, this review will mainly focus on analysing the basic components of the gut that might be responsible for aggravating lewy pathology, the mediator(s) responsible for transmission of PD pathology from gut to brain and the important role of trehalose in ameliorating gut dysbiosis related PD complications that would eventually pave the way for therapeutic

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Genetic Approaches Using Zebrafish to Study the Microbiota–Gut–Brain Axis in Neurological Disorders

Gut Dysbiosis, Gut Microbiota, Vagal Nerve /

The microbiota–gut–brain axis (MGBA) is a bidirectional signaling pathway mediating the interaction of the microbiota, the intestine, and the central nervous system. While the MGBA plays a pivotal role in normal development and physiology of the nervous and gastrointestinal system of the host, its dysfunction has been strongly implicated in neurological disorders, where intestinal dysbiosis

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CSF Biomarker Flags Parkinson’s Pathology Years Before Symptoms Appear

A-Synuclein, Biomarkers, iRBD, Pre-PD, Vagal Nerve /

Real-time quaking-induced conversion (RT-QuIC), a test for pathological misfolded protein, detected alpha-synuclein in the cerebrospinal fluid (CSF) of patients with isolated rapid-eye-movement (REM) sleep behavior disorder (IRBD), years before clinical symptoms of Parkinson’s disease or dementia with Lewy bodies emerged. In these patients, RT-QuIC detected misfolded alpha-synuclein in CSF with both sensitivity and specificity of

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Cross-seeding of alpha-synuclein aggregation by amyloid fibrils of food proteins

A-Synuclein, ENS, Vagal Nerve /

In this work, we investigated the ability of amyloid fibrils derived from two food proteins to heterologously seed the aggregation of the PD-related aSyn protein. While β-lactoglobulin amyloid fibril seeds were not able to induce aSyn aggregation, we identified a fibril surface–mediated nucleation mechanism for the seeding of aSyn aggregation by hen egg white lysozyme

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Lactobacillus plantarum PS128 Ameliorated Visceral Hypersensitivity in Rats Through the Gut–Brain Axis

Constipation, Gut-Brain axis, Pre-PD, Probiotics, Prebiotics and Symbiotics, Vagal Nerve /

The hypothalamic–pituitary–adrenal axis was modulated by PS128 with decreased corticosterone concentration in serum and the expression of mineralocorticoid receptors in the amygdala. Oral administration of PS128 inhibited 5-HTPinduced VH during CRD. The ameliorative effect on VH suggests the potential application of PS128 for IBS. CLICK TO REVIEW

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