On cell loss in Parkinson’s disease, and the citations that followed

Nanni, Samuel Burke; Trudeau, Louis-Éric

doi:10.1038/s41531-022-00306-x

Cited by 2 publications

(2 citation statements)

References 15 publications

(10 reference statements)

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“…S11M ) ( 24 , 25 ). This Confirm previous observations in PD patients ( 26 , 27 ), where increased accumulation of alpha-synuclein in the LDTg and the DR correlated with sleep disorders and depressive-like phenotypes ( 28 , 29 ).…”

Section: Resultssupporting

confidence: 92%

Gut-Initiated Alpha Synuclein Fibrils Drive Parkinson's Disease Phenotypes: Temporal Mapping of non-Motor Symptoms and REM Sleep Behavior Disorder

Dautan,

Paslawski,

Montejo

et al. 2024

Preprint

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Parkinson's disease (PD) is characterized by progressive motor as well as less recognized non-motor symptoms that arise often years before motor manifestation, including sleep and gastrointestinal disturbances. Despite the heavy burden on the patient's quality of life, these non-motor manifestations are poorly understood. To elucidate the temporal dynamics of the disease, we employed a mouse model involving injection of alpha-synuclein (aSyn) pre-formed fibrils (PFF) in the duodenum and antrum as a gut-brain model of Parkinsonism. Using anatomical mapping of aSyn-PFF propagation and behavioral and physiological characterizations, we unveil a correlation between post-injection time the temporal dynamics of aSyn propagation and non-motor/motor manifestations of the disease. We highlight the concurrent presence of aSyn aggregates in key brain regions, expressing acetylcholine or dopamine, involved in sleep duration, wakefulness, and particularly REM-associated atonia corresponding to REM behavioral disorder-like symptoms. This study presents a novel and in-depth exploration into the multifaceted nature of PD, unraveling the complex connections between aSynucleinopathies, gut-brain connectivity, and the emergence of non-motor phenotypes.

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Section: Resultssupporting

confidence: 92%

Gut-Initiated Alpha Synuclein Fibrils Drive Parkinson's Disease Phenotypes: Temporal Mapping of non-Motor Symptoms and REM Sleep Behavior Disorder

Dautan,

Paslawski,

Montejo

et al. 2024

Preprint

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show abstract

“…Previously, we introduced sFIDA as a protein oligomer-specific quantification method for counting single proteinaceous particles. sFIDA features a combination of an ELISA-like biochemical setup and microscopy-based readout with sub-femtomolar sensitivity [11][12][13][14] . In the hereby for DISC1 perotein aggregates adapted sFIDA assay, samples are incubated on a capture antibody-coated glass surface and both monomeric and aggregated DISC1 species are immobilized.…”

Section: Disc1 In Csfmentioning

confidence: 99%

Disrupted-in-schizophrenia 1 (DISC1) protein aggregates in cerebrospinal fluid are elevated in first-episode psychosis patients

Pils

Rutsch

Eren

et al. 2023

Preprint

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The Disrupted-in-schizophrenia 1 (DISC1) protein is a key regulator at the intersection of signaling pathways relevant for adaptive behavior. It is prone to posttranslational changes such as misassembly and aggregation but the significance of such transformations for human mental illness has remained unclear. Here we demonstrate that DISC1 protein aggregates are increased in CSF samples of patients with first episode psychosis (n=50) compared to healthy controls (n=47), as measured by the highly sensitive surface-based fluorescence intensity distribution analysis technology that enables single aggregate detection. The concentration was in the low femtomolar range. No correlations were found to symptom levels, but the difference was particularly significant in the subset of patients receiving the diagnoses schizophrenia, unspecified (DSM IV 295.9) or schizoaffective disorder (DSM IV 295.70) at 18-month follow-up. The occurrence of protein aggregates in vivo in patients with psychotic disorders has not been previously reported. It underscores the significance of posttranslational modifications of proteins both as pathogenetic mechanisms and as potential diagnostic markers in these disorders.

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On cell loss in Parkinson’s disease, and the citations that followed

Cited by 2 publications

References 15 publications

Gut-Initiated Alpha Synuclein Fibrils Drive Parkinson's Disease Phenotypes: Temporal Mapping of non-Motor Symptoms and REM Sleep Behavior Disorder

Gut-Initiated Alpha Synuclein Fibrils Drive Parkinson's Disease Phenotypes: Temporal Mapping of non-Motor Symptoms and REM Sleep Behavior Disorder

Disrupted-in-schizophrenia 1 (DISC1) protein aggregates in cerebrospinal fluid are elevated in first-episode psychosis patients

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