Olfactory

Loss of ones sense of smell

Dual role of the nasal microbiota in neurological diseases—An unignorable risk factor or a potential therapy carrier

Gut Dysbiosis, Mitochondria, Olfactory, Parkinson's Disease /

Recently, comparative studies have rapidly increased with the closer correlation between microbiota and neurological diseases. However, most insights about the association between microbiota and neurological diseases still focus on the gut-brain axis and ignore that nasal microbiota could form a complex and essential link with the nervous system via the nose-to-brain pathway, suggesting the role […]

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Environmental triggers of Parkinson’s disease – Implications of the Braak and dual-hit hypotheses

A-Synuclein, Biomarkers, Gut Dysbiosis, Gut Permeability / Leaky Gut, Gut-Brain axis, Olfactory, Parkinson's Disease, Pre-PD /

Idiopathic Parkinson’s disease (PD) may take decades to develop, during which many risk or protective factors may come into play to initiate the pathogenesis or modify its progression to clinical PD. The lack of understanding of this prodromal phase of PD and the factors involved has been a major hurdle in the study of PD

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α-Synuclein aggregation in the olfactory bulb induces olfactory deficits by perturbing granule cells and granular–mitral synaptic transmission

A-Synuclein, Olfactory, Parkinson's Disease, Pre-PD /

Olfactory dysfunction is an early pre-motor symptom of Parkinson’s disease (PD) but the neural mechanisms underlying this dysfunction remain largely unknown. Aggregation of α-synuclein is observed in the olfactory bulb (OB) during the early stages of PD, indicating a relationship between α-synuclein pathology and hyposmia. Here we investigate whether and how α-synuclein aggregates modulate neural

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Deep nasal sinus cavity microbiota dysbiosis in Parkinson’s disease

Olfactory /

Olfactory dysfunction is a pre-motor symptom of Parkinson’s disease (PD) that appears years prior to diagnosis and can affect quality of life in PD. Changes in microbiota community in deep nasal cavity near the olfactory bulb may trigger the olfactory bulb-mediated neuroinflammatory cascade and eventual dopamine loss in PD. To determine if the deep nasal

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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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Olfactory dysfunction in aging and neurodegenerative diseases

Biomarkers, Dementia - Lewy Bodies, Olfactory /

The establishment of biomarkers that promote early risk identification is critical for the implementation of early treatment to postpone or avert pathological development. Olfactory dysfunction (OD) is seen in 90% of early-stage PD patients and 85% of patients with early-stage AD, which makes it an attractive biomarker for early diagnosis of these diseases. Here, we

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Biomonitoring of Mycotoxins in Plasma of Patients with Alzheimer’s and Parkinson’s Disease

Gut Microbiota, Mold, Mycotoxins, Olfactory, Parkinson's Disease /

In the case of PD, the fact that the disease is accompanied by other non-motor symptoms in organs highly exposed to the environment (olfactory and gastrointestinal systems) reinforces the hypotheses of the role of environmental factors in the etiology of PD. Many chemicals such as pesticides, metals (iron and lead), polychlorinated biphenyls, solvents such as

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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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