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001     169044
005     20250127111029.0
024 7 _ |a 1545-5343
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024 7 _ |a 10.1007/s13311-022-01332-6
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024 7 _ |a 1933-7213
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024 7 _ |a 1545-5351
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037 _ _ |a DZNE-2022-01766
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Pinto-Costa, Rita
|0 P:(DE-2719)9001609
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245 _ _ |a Overexpression-Induced α-Synuclein Brain Spreading.
260 _ _ |a New York, NY
|c 2023
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520 _ _ |a Interneuronal transfer of pathological α-synuclein species is thought to play an important role in the progressive advancement of Lewy pathology and increasing severity of clinical manifestations in Parkinson's and other diseases commonly referred to as synucleinopathies. Pathophysiological conditions and mechanisms triggering this trans-synaptic spreading bear therefore significant pathogenetic implications but have yet to be fully elucidated. In vivo experimental models support the conclusion that increased expression of intraneuronal α-synuclein can itself induce protein spreading throughout the brain as well as from the brain to peripheral tissues. For example, overexpression of α-synuclein targeted to the rodent dorsal medulla oblongata results in its transfer and accumulation into recipient axons innervating this brain region; through these axons, α-synuclein can then travel caudo-rostrally and reach other brain sites in the pons, midbrain, and forebrain. When protein overexpression is induced in the rodent midbrain, long-distance α-synuclein spreading can be followed over time; spreading-induced α-synuclein accumulation affects lower brain regions, including the dorsal motor nucleus of the vagus, proceeds through efferent axons of the vagus nerve, and is ultimately detected within vagal motor nerve endings in the gastric wall. As discussed in this review, animal models featuring α-synuclein overexpression not only support a relationship between α-synuclein burden and protein spreading but have also provided important clues on conditions/mechanisms capable of promoting interneuronal α-synuclein transfer. Intriguing findings include the relationship between neuronal activity and protein spreading and the role of oxidant stress in trans-synaptic α-synuclein mobility.
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650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a alpha-Synuclein: metabolism
|2 MeSH
650 _ 2 |a Brain: metabolism
|2 MeSH
650 _ 2 |a Neurons: metabolism
|2 MeSH
650 _ 2 |a Parkinson Disease: metabolism
|2 MeSH
650 _ 2 |a Stomach: innervation
|2 MeSH
650 _ 2 |a Stomach: metabolism
|2 MeSH
650 _ 2 |a Synaptic Transmission: physiology
|2 MeSH
650 _ 2 |a Synucleinopathies: metabolism
|2 MeSH
650 _ 2 |a Vagus Nerve: metabolism
|2 MeSH
650 _ 2 |a Vagus Nerve: physiology
|2 MeSH
650 _ 7 |a alpha-Synuclein
|2 NLM Chemicals
650 _ 7 |a Animal models
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650 _ 7 |a Gut-brain axis
|2 Other
650 _ 7 |a Neuronal activity
|2 Other
650 _ 7 |a Oxidative stress
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650 _ 7 |a Parkinson
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650 _ 7 |a Vagus nerve
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700 1 _ |a Harbachova, Eugenia
|0 P:(DE-2719)9001593
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|u dzne
700 1 _ |a La Vitola, Pietro
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700 1 _ |a Di Monte, Donato Antonio
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773 _ _ |a 10.1007/s13311-022-01332-6
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|p 83-96
|t Neurotherapeutics
|v 20
|y 2023
|x 1933-7213
856 4 _ |u https://pub.dzne.de/record/169044/files/DZNE-2022-01766.pdf
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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