{'fraction_non_alphanumeric': 0.030031948881789138, 'fraction_numerical': 0.010223642172523962, 'mean_word_length': 5.552301255230126, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Peripheral and central respiratory system pathology in a mouse model of Parkinson's disease: A prodromal signature of clinical relevance?

Parkinson ' s disease (PD) is a debilitating neurodegenerative disease characterized by progressive motor impairment, with physical symptoms that include resting tremor, muscle rigidity and impaired voluntary movement, balance and posture. Non-motor consequences of PD include depression, anxiety and dementia, in addition to disturbed emotional and sleep states. Mid-brain dopaminergic neuronal cell death is a hallmark of PD, a consequence of Lewy body and Lewy neurite aggregation that result from the abnormal accumulation of 𝛼 -synuclein. In this issue of Experimental Physiology , Oliveira, Oliveira, Moriya, Moreira, and Takakura (2019) describe new findings in a mouse model of PD focused on neuropathology in medullary respiratory control circuits and aberrant respiratory control and mechanics. In adult male mice, 6-hydroxydopamine (6-OHDA) was administered bilaterally into the striatum to induce nigrostriatal injury, confirmed after 40 days with evidence of a ∼ 70% reduction in the population of tyrosine hydroxylase-expressing neurons in the substantia nigra pars compacta (SNpc), sparing catecholaminergic neurons of the C1 region of the medulla oblongata and A6 region of the pons. Forty days after SNpc insult with 6-OHDA, immunohistochemical assessment revealed a ∼ 31% reduction in neurokinin-1 receptor density in the pre-B ӧ tzinger complex of the medulla, a site crucial for respiratory rhythmogenesis.