Dermal p-syn in iRBD is most probably an early consistent marker of synucleinopathy and may support other indicators of conversion to manifest disease state. CLICK TO REVIEW
This review aims to provide an insight into the current literature concerning salivary biomarkers used in the diagnosis of AD and PD. The most commonly studied salivary biomarkers in AD are β-amyloid1-42/1-40 and TAU protein, as well as α-synuclein and protein deglycase (DJ-1) in PD. Studies continue to be conducted on this subject and researchers
Real-time quaking-induced conversion (RT-QuIC), a test for pathological misfolded protein, detected alpha-synuclein in the cerebrospinal fluid (CSF) of patients with isolated rapid-eye-movement (REM) sleep behavior disorder (IRBD), years before clinical symptoms of Parkinson’s disease or dementia with Lewy bodies emerged. In these patients, RT-QuIC detected misfolded alpha-synuclein in CSF with both sensitivity and specificity of
CSF Biomarker Flags Parkinson’s Pathology Years Before Symptoms Appear Read More »
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
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
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
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
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 »
Sleep Disorders (SDs) precede motor symptoms of Parkinson’s disease (PD), suggesting an early effect of disease processes on sleep control neurons. These nucleus-specific differential effects suggest previously unappreciated, mechanistic underpinnings of SDs’ prodromal PD appearance in PD, and wehypothesize that in the prodromal phase of PD, the early form of α-synuclein compromises sleep-control neurons. https://doi.org/10.21203/rs.3.rs-134060/v1