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000278657 1001_ $$0P:(DE-2719)9002553$$aSzegő, Éva M$$b0$$eFirst author
000278657 245__ $$aIntermittent fasting reduces alpha-synuclein pathology and functional decline in a mouse model of Parkinson's disease.
000278657 260__ $$a[London]$$bSpringer Nature$$c2025
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000278657 520__ $$aParkinson's disease (PD) is a neurodegenerative disorder characterized by dopaminergic neuron degeneration and α-synuclein (aSyn) accumulation. Environmental factors play a significant role in PD progression, highlighting the potential of non-pharmacological interventions. This study investigates the therapeutic effects of intermittent fasting (IF) in an rAAV-aSyn mouse model of PD. IF, initiated four weeks post-induction of aSyn pathology, improved motor function and reduced dopaminergic neuron and axon terminal degeneration. Additionally, IF preserved dopamine levels and synaptic integrity in the striatum. Mechanistically, IF enhanced autophagic activity, promoting phosphorylated-aSyn clearance and reducing its accumulation in insoluble brain fractions. Transcriptome analysis revealed IF-induced modulation of inflammation-related genes and microglial activation. Validation in primary cultures confirmed that autophagy activation and inflammatory modulators (CCL17, IL-36RN) mitigate aSyn pathology. These findings suggest that IF exerts neuroprotective effects, supporting further exploration of IF and IF-mimicking therapies as potential PD treatments.
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000278657 650_7 $$2NLM Chemicals$$aalpha-Synuclein
000278657 650_7 $$0VTD58H1Z2X$$2NLM Chemicals$$aDopamine
000278657 650_2 $$2MeSH$$aAnimals
000278657 650_2 $$2MeSH$$aalpha-Synuclein: metabolism
000278657 650_2 $$2MeSH$$aalpha-Synuclein: genetics
000278657 650_2 $$2MeSH$$aParkinson Disease: metabolism
000278657 650_2 $$2MeSH$$aParkinson Disease: pathology
000278657 650_2 $$2MeSH$$aParkinson Disease: therapy
000278657 650_2 $$2MeSH$$aParkinson Disease: genetics
000278657 650_2 $$2MeSH$$aFasting: physiology
000278657 650_2 $$2MeSH$$aDisease Models, Animal
000278657 650_2 $$2MeSH$$aMice
000278657 650_2 $$2MeSH$$aDopaminergic Neurons: metabolism
000278657 650_2 $$2MeSH$$aDopaminergic Neurons: pathology
000278657 650_2 $$2MeSH$$aMale
000278657 650_2 $$2MeSH$$aAutophagy
000278657 650_2 $$2MeSH$$aMice, Inbred C57BL
000278657 650_2 $$2MeSH$$aDopamine: metabolism
000278657 650_2 $$2MeSH$$aHumans
000278657 650_2 $$2MeSH$$aCorpus Striatum: metabolism
000278657 650_2 $$2MeSH$$aCorpus Striatum: pathology
000278657 650_2 $$2MeSH$$aMicroglia: metabolism
000278657 650_2 $$2MeSH$$aIntermittent Fasting
000278657 7001_ $$0P:(DE-2719)9002445$$aHöfs, Lennart$$b1$$udzne
000278657 7001_ $$0P:(DE-2719)2812905$$aAntoniou, Anna$$b2$$udzne
000278657 7001_ $$0P:(DE-2719)9001016$$aDinter, Elisabeth$$b3$$udzne
000278657 7001_ $$00000-0002-3188-8431$$aBernhardt, Nadine$$b4
000278657 7001_ $$0P:(DE-2719)2812035$$aSchneider, Anja$$b5
000278657 7001_ $$0P:(DE-2719)2481741$$aDi Monte, Donato A$$b6
000278657 7001_ $$0P:(DE-2719)2814178$$aFalkenburger, Björn$$b7$$eLast author$$udzne
000278657 773__ $$0PERI:(DE-600)2553671-0$$a10.1038/s41467-025-59249-5$$gVol. 16, no. 1, p. 4470$$n1$$p4470$$tNature Communications$$v16$$x2041-1723$$y2025
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