A-Synuclein

Spectrum of Non-Motor Symptoms in Parkinson’s Disease

A-Synuclein, Biomarkers, Gut Dysbiosis, iRBD, Olfactory, Pre-PD /

Parkinson’s disease is predominantly classified as a movement disorder. Beyond the textbook definition of rigidity, tremors, and bradykinesia, Parkinson’s disease encompasses an entire entity of non-motor symptom complexes that can precede the motor features by many years. Despite their significant clinical importance, the awareness of non-motor symptoms is quite negligible. Sleep disorders, gastrointestinal dysfunction, olfactory […]

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REST protects dopaminergic neurons from mitochondrial and α-synuclein oligomer pathology in an alpha synuclein overexpressing BAC-transgenic mouse model

A-Synuclein /

Finally, decreased α-synuclein oligomer accumulation and mitochondrial dysfunction in mice correlated with nuclear REST and PGC-1α in protected SN GABAergic neurons, when compared to vulnerable dopaminergic neurons. Our findings show that increased levels of α-synuclein oligomers cause dopaminergic neuronal-specific dysfunction through mitochondrial toxicity, which can be attenuated by REST in an early model of Parkinsonian

REST protects dopaminergic neurons from mitochondrial and α-synuclein oligomer pathology in an alpha synuclein overexpressing BAC-transgenic mouse model Read More »

Marker-free imaging of α-Synuclein aggregates in a rat model of
2 Parkinson’s disease using Raman microspectroscopy

A-Synuclein, Biomarkers, Pre-PD /

A hallmark of Parkinson’s disease (PD) is the formation of Lewy bodies in the brain. Lewy bodies are rich in the aggregated form of misfolded α-Synuclein (α-Syn). The brain from PD patients can only be analysed after post-mortem, limiting the diagnosis of PD to the manifestation of motor symptoms. In PD patients and animal models

Marker-free imaging of α-Synuclein aggregates in a rat model of
2 Parkinson’s disease using Raman microspectroscopy Read More »

Expression Levels of an Alpha-Synuclein Transcript in Blood May Distinguish between Early Dementia with Lewy Bodies and Parkinson’s Disease

A-Synuclein /

In conclusion, SNCA transcripts showed a disease-specific increase in the brain and were diminished in blood of LBD patients. SNCAtv3 expression was decreased in early DLB and increased in early PD and could be a biomarker for early DLB diagnosis. CLICK TO REVIEW

Expression Levels of an Alpha-Synuclein Transcript in Blood May Distinguish between Early Dementia with Lewy Bodies and Parkinson’s Disease Read More »

Alpha-Synuclein: The Interplay of Pathology, Neuroinflammation, and Environmental Factors in Parkinson’s Disease

A-Synuclein, Gut-Brain axis /

Background: Parkinson’s disease (PD) is a multifactorial, chronic, and progressive neurodegenerative disease. α-Synuclein (α-syn), which is the main protein component of Lewy bodies, plays an important role in the pathological hallmarks of PD. However, the pathological function of α-syn and the molecular mechanisms responsible for the degeneration of dopaminergic neurons are still elusive. Summary: Cumulative evidence implicates that

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Achieving brain clearance and preventing neurodegenerative diseases—A glymphatic perspective

A-Synuclein /

The glymphatic system is involved in clearance of metabolic byproducts such as amyloid-b from the brain, and its function is believed to lower the risk of developing some of the most common neurodegenerative diseases. Here, we present magnetic resonance imaging (MRI) data on the heart cycle’s control of CSF flow in humans which corroborates findings

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How microcompetition with latent viruses can cause α synuclein aggregation, mitochondrial dysfunction, and eventually Parkinson’s disease

A-Synuclein, Mitochondria, Viral / Bacterial Infections /

The cause of most Parkinson’s disease cases is unknown. However, it is well documented that mitochondrial dysfunction and misfolded α synuclein aggregation are important cellular abnormalities associated with the disease. In this paper, we use the microcompetition model to show how latent viruses, which infect the central and peripheral nervous systems, can cause the observed mitochondrial dysfunction

How microcompetition with latent viruses can cause α synuclein aggregation, mitochondrial dysfunction, and eventually Parkinson’s disease Read More »

Probiotic Bacillus subtilis Protects against a-Synuclein Aggregation in C. elegans

A-Synuclein, Probiotics, Prebiotics and Symbiotics /

Recent discoveries have implicated the gut microbiome in the progression and severity of Parkinson’s disease; however, how gut bacteria affect such neurodegenerative disorders remains unclear. Here, we report that the Bacillus subtilis probiotic strain PXN21 inhibits a synuclein aggregation and clears preformed aggregates in an established Caenorhabditis elegans model of synucleinopathy. CLICK TO REVIEW

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Pathophysiology of Parkinson’s disease:
Mitochondria, alpha-synuclein and much more. . .

A-Synuclein, Gut-Brain axis, Mitochondria /

ABSTRACT: Here, we give an overview of the progress that has been made over the past four decades in our understanding of this disorder. We review the role of mitochondria, environmental toxicants, alpha-synuclein and neuroinflammation in the development of PD. We also discuss more recent data from genetics, which strongly support the endosomal-lysosomal pathways and

Pathophysiology of Parkinson’s disease:
Mitochondria, alpha-synuclein and much more. . . Read More »