scholarly journals Abnormal Vision-Based Displacement Perception in Parkinson’s Disease

2021 ◽  
Vol 15 ◽  
Author(s):  
Matthew Bernardinis ◽  
S. Farokh Atashzar ◽  
Rajni V. Patel ◽  
Mandar S. Jog
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Visual Processing ◽  
De Novo ◽  
Early Stage ◽  
Absolute Measurement ◽  
Motor Disorder ◽  
Independent Manner ◽  
Graphical Tool ◽  
Wide Range

In this work, we investigate the effect of Parkinson’s disease (PD), and common corresponding therapies on vision-based perception of motion, a critical perceptual ability required for performing a wide range of activities of daily livings. While PD has been recognized as mainly a motor disorder, sensory manifestation of PD can also play a major role in the resulting disability. In this paper, for the first time, the effect of disease duration and common therapies on vision-based perception of displacement were investigated. The study is conducted in a movement-independent manner, to reject the shadowing effects and isolate the targeted perceptual disorder to the maximum possible extent. Data was collected using a computerized graphical tool on 37 PD patients [6 early-stage de novo, 25 mid-stage using levodopa therapy, six later-stage using deep brain stimulation (DBS)] and 15 control participants. Besides the absolute measurement of perception through a psychometric analysis on two tested position reference magnitudes, we also investigated the linearity in perception using Weber’s fraction. The results showed that individuals with PD displayed significant perceptual impairments compared to controls, though early-stage patients were not impaired. Mid-stage patients displayed impairments at the greater of the two tested reference magnitudes, while late-stage patients were impaired at both reference magnitudes. Levodopa and DBS use did not cause statistically significant differences in absolute displacement perception. The findings suggest abnormal visual processing in PD increasing with disease development, perhaps contributing to sensory-based impairments of PD such as bradykinesia, visuospatial deficits, and abnormal object recognition.

Association of the Non-Motor Burden with Patterns of Striatal Dopamine Loss in de novo Parkinson’s Disease

2020 ◽  
Vol 10 (4) ◽  
pp. 1541-1549
Author(s):  
Seok Jong Chung ◽  
Sangwon Lee ◽  
Han Soo Yoo ◽  
Yang Hyun Lee ◽  
Hye Sun Lee ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
De Novo ◽  
Early Stage ◽  
Striatal Dopamine ◽  
Motor Deficits ◽  
Dopamine Depletion ◽  
Severe Motor ◽  
Severe Group ◽  
Striatal Dopamine Depletion

Background: Striatal dopamine deficits play a key role in the pathogenesis of Parkinson’s disease (PD), and several non-motor symptoms (NMSs) have a dopaminergic component. Objective: To investigate the association between early NMS burden and the patterns of striatal dopamine depletion in patients with de novo PD. Methods: We consecutively recruited 255 patients with drug-naïve early-stage PD who underwent 18F-FP-CIT PET scans. The NMS burden of each patient was assessed using the NMS Questionnaire (NMSQuest), and patients were divided into the mild NMS burden (PDNMS-mild) (NMSQuest score <6; n = 91) and severe NMS burden groups (PDNMS-severe) (NMSQuest score >9; n = 90). We compared the striatal dopamine transporter (DAT) activity between the groups. Results: Patients in the PDNMS-severe group had more severe parkinsonian motor signs than those in the PDNMS-mild group, despite comparable DAT activity in the posterior putamen. DAT activity was more severely depleted in the PDNMS-severe group in the caudate and anterior putamen compared to that in the PDMNS-mild group. The inter-sub-regional ratio of the associative/limbic striatum to the sensorimotor striatum was lower in the PDNMS-severe group, although this value itself lacked fair accuracy for distinguishing between the patients with different NMS burdens. Conclusion: This study demonstrated that PD patients with severe NMS burden exhibited severe motor deficits and relatively diffuse dopamine depletion throughout the striatum. These findings suggest that the level of NMS burden could be associated with distinct patterns of striatal dopamine depletion, which could possibly indicate the overall pathological burden in PD.

scholarly journals Ocular fixations and presaccadic potentials to explain pareidolias in Parkinson’s disease

2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Gajanan S Revankar ◽  
Noriaki Hattori ◽  
Yuta Kajiyama ◽  
Tomohito Nakano ◽  
Masahito Mihara ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Eye Tracking ◽  
Eye Movement ◽  
Visual Processing ◽  
Top Down ◽  
Scalp Eeg ◽  
Wide Range ◽  
Saccade Size ◽  
Global And Local

Abstract In Parkinson’s disease, a precursor phenomenon to visual hallucinations presents as ‘pareidolias’ which make ambiguous forms appear meaningful. To evoke and detect pareidolias in patients, a noise pareidolia test was recently developed, although its task-dependent mechanisms are yet to be revealed. When subjected to this test, we hypothesized that patients exhibiting pareidolias would show altered top-down influence of visual processing allowing us to demonstrate the influence of pareidolic illusionary behaviour in Parkinson’s disease patients. To that end, we evaluated eye-movement strategies and fixation-related presaccadic activity on scalp EEG when participants performed the test. Twelve healthy controls and 21 Parkinson’s disease patients, evaluated for cognitive, visuo-spatial and executive functions, took a modified computer-based version of the noise pareidolia test in a free-viewing EEG eye-tracking experiment. Eye-tracking metrics (fixation-related durations and counts) documented the eye movement behaviour employed in correct responses (face/noise) and misperceptions (pareidolia/missed) during early and late visual search conditions. Simultaneously, EEG recorded the presaccadic activity in frontal and parietal areas of the brain. Based on the noise pareidolia test scores, we found certain Parkinson’s disease patients exhibited pareidolias whereas others did not. ANOVA on eye-tracking data showed that patients dwelled significantly longer to detect faces and pareidolias which affected both global and local search dynamics depending on their visuo-perceptual status. Presaccadic activity in parietal electrodes for the groups was positive for faces and pareidolias, and negative for noise, though these results depended mainly on saccade size. However, patients sensitive to pareidolias showed a significantly higher presaccadic potential on frontal electrodes independent of saccade sizes, suggesting a stronger frontal activation for pareidolic stimuli. We concluded with the following interpretations (i) the noise pareidolia test specifically characterizes visuo-perceptual inadequacies in patients despite their wide range of cognitive scores, (ii) Parkinson’s disease patients dwell longer to converge attention to pareidolic stimuli due to abnormal saccade generation proportional to their visuo-perceptual deficit during early search, and during late search, due to time-independent alteration of visual attentional network and (iii) patients with pareidolias show increased frontal activation reflecting the allocation of attention to irrelevant targets that express the pareidolic phenomenon. While the disease per se alters the visuo-perceptual and oculomotor dynamics, pareidolias occur in Parkinson’s disease due to an abnormal top-down modulation of visual processing that affects visual attention and guidance to ambiguous stimuli.

scholarly journals P.015 Long-term progression and prognosis in different subtypes of Parkinson’s disease: validation of a new multi-domain subtyping method

2019 ◽  
Vol 46 (s1) ◽  
pp. S17
Author(s):  
S Fereshtehnejad ◽  
Y Zeighami ◽  
A Dagher ◽  
RB Postuma
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
De Novo ◽  
Early Stage ◽  
Real Life ◽  
Clinical Manifestations ◽  
Personalized Care ◽  
Autonomic Disturbance ◽  
Progression Markers

Background: Parkinson’s disease (PD) varies in clinical manifestations and course of progression from person to person. Identification of distinct PD subtypes is of great priority to develop personalized care approaches. We aimed to compare long-term progression and prognosis between different PD subtypes. Methods: Data on 421 individuals with de novo early-onset PD was retrieved from Parkinson’s Progression Markers Initiative (PPMI). Using a newly developed multi-domain subtyping method (based on motor phenotype, RBD, autonomic disturbance, early cognitive deficit), we divided PD population into three subtypes at baseline: “mild motor-predominant”, “Diffuse malignant” and “Intermediate”. Rate of global progression (mixed motor and non-motor features) and developing dementia were compared between the subtypes. Results: Patients with “diffuse malignant” PD experienced 0.5 z-score further worsening of global composite outcome (p=0.017) and 2.2 further decline in MOCA score (p=0.001) after 6-years of follow-up. Hazard for MCI/dementia was significantly higher in “diffuse malignant” (HR=3.2, p&lt;0.001) and “intermediate” (HR=1.8, p&lt;0.001) subtypes. Individuals with “diffuse malignant” PD had the lowest level of CSF amyloid-beta (p=0.006) and SPECT striatal binding ratio (p=0.001). Conclusions: This multi-domain subtyping is a valid method to predict subgroups of PD with distinct patterns of long-term progression at drug-naïve early-stage with potential application in real-life clinical practice.

scholarly journals Dopamine replacement remediates risk aversion in Parkinson’s disease in a value-independent manner

2019 ◽  
Author(s):  
Mariya V. Cherkasova ◽  
Jeffrey C. Corrow ◽  
Alisdair Taylor ◽  
Shanna C. Yeung ◽  
Jacob L. Stubbs ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Risk Aversion ◽  
Risk Tolerance ◽  
Independent Manner ◽  
A Value ◽  
Wide Range ◽  
Reward Value ◽  
Expected Values ◽  
Gain Frame

ABSTRACTIntroductionClinical evidence suggests that Parkinson’s Disease (PD) patients are risk averse. Dopaminergic therapy has been reported to increase risk tolerance, but the underlying mechanisms are unclear. Some studies have suggested an amplification of subjective reward value, consistent with the role of dopamine in reward value coding. Others have reported value-independent risk enhancement. We evaluated the value-dependence of the effects of PD and its therapy on risk using tasks designed to sensitively measure risk over a wide range of expected values.Method36 patients with idiopathic PD receiving levodopa monotherapy and 36 healthy matched controls performed two behavioural economic tasks aimed at quantifying 1) risk tolerance/ aversion in the gain frame and 2) valuation of potential gains relative to losses. PD patients performed the tasks on and off their usual dose of levodopa in randomized order; controls performed the same tasks twice.ResultsRelative to the controls, unmedicated PD patients showed significant value-independent risk aversion in the gain frame, which was normalized by levodopa. PD patients did not differ from controls in their valuation of gains relative to losses. However, across both tasks and regardless of medication, choices of the patients were more determined by expected values of the prospects than those of controls.ConclusionDopamine deficiency in PD was associated with risk aversion, and levodopa promoted riskier choice in a value-independent manner. PD patients also showed an increased sensitivity to expected value, which was independent of levodopa and does not appear to result directly from dopamine deficiency.

scholarly journals Extending our Understanding of the Dopaminergic Basis of Non-motor Symptoms in Parkinson’s Disease

2015 ◽  
Vol 10 (01) ◽  
pp. 23 ◽  
Author(s):  
Amos D Korczyn ◽  
K Ray Chaudhuri ◽  
Teus van Laar ◽  
◽  
◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cognitive Impairment ◽  
Sleep Problems ◽  
Disease Process ◽  
Motor Symptom ◽  
Motor Disorder ◽  
Motor Symptoms ◽  
Wide Range ◽  
Non Motor Symptoms

Parkinson’s disease (PD) is primarily considered as a motor disorder but there is increasing recognition of the wide range of non-motor symptoms (NMS), such as low mood, pain, apathy, fatigue and sleep problems, which may be experienced by PD patients across the spectrum of the disease. Notably, NMS often occur before motor symptoms develop and are known to place a significant burden on health-related quality of life (HRQoL) of the person with PD. Commonly, NMS go undiagnosed by the clinician and are therefore undertreated; however, to optimise patient outcomes, both motor and non-motor aspects of PD need to be recognised and managed effectively. The 10th International Congress on Non-Motor Dysfunctions in Parkinson’s Disease and Related Disorders held in Nice, France, in December 2014, offered the opportunity to look further into the dopaminergic basis of NMS and how this may affect clinical management. Britannia arranged an international faculty, chaired by Professor Amos Korczyn (Tel Aviv, Israel), to review the latest developments in our understanding of the underlying aetiology and clinical burden of non-motor features in PD that will ultimately help inform clinical practice. Surveys indicate that NMS have an extremely high prevalence among PD patients and evidence now suggests that it is the total ‘burden’ of NMS, combining frequency and severity, and not just the occurrence of individual NMS such as depression, which is the major determinant of a patient’s HRQoL. Recognising the significant contribution of NMS to the total clinical picture in PD, in order to provide a more comprehensive grading of PD severity, it is now proposed that the clinical assessment of PD patients needs a combined approach using for example the validated Non-motor Symptoms Scale (NMSS) to assess total NMS burden in addition to classic motor symptom scoring. Recent data from newly diagnosed PD patients also suggests there are different subtypes of PD that may have implications for both clinical trial design and the selection of therapy. Cognitive impairment often occurs in patients with PD, even in early disease, progressing to PD dementia in a substantial proportion of patients, which can limit therapeutic options. Posterior cortical dysfunction is a negative predictor of the progression of PD with mild cognitive impairment to PD dementia. Pronounced nigrostriatal denervation is characteristic of PD; however, cholinergic changes are also observed. Cholinergic depletion starts early in the disease process and by the time PD dementia develops patients will have a significant cholinergic deficit in various cortical regions. Current research is focused on the potential to reduce cognitive decline by decreasing beta-amyloid plaques.

scholarly journals Differential Temporal Perception Abilities in Parkinson’s Disease Patients Based on Timing Magnitude

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Matthew Bernardinis ◽  
S. Farokh Atashzar ◽  
Mandar S. Jog ◽  
Rajni V. Patel
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
De Novo ◽  
Interval Timing ◽  
Internal Clock ◽  
Temporal Perception ◽  
Motor Symptoms ◽  
Strong Trend ◽  
Graphical Tool ◽  
Timing Processes

AbstractNon-motor symptoms in Parkinson’s Disease (PD) predate motor symptoms and substantially decrease quality of life; however, detection, monitoring, and treatments are unavailable for many of these symptoms. Temporal perception abnormalities in PD are generally attributed to altered Basal Ganglia (BG) function. Present studies are confounded by motor control facilitating movements that are integrated into protocols assessing temporal perception. There is uncertainty regarding the BG’s influence on timing processes of different time scales and how PD therapies affect this perception. In this study, PD patients using Levodopa (n = 25), Deep Brain Stimulation (DBS; n = 6), de novo patients (n = 6), and healthy controls (n = 17) completed a visual temporal perception task in seconds and sub-section timing scales using a computer-generated graphical tool. For all patient groups, there were no impairments seen at the smaller tested magnitudes (using sub-second timing). However, all PD groups displayed significant impairments at the larger tested magnitudes (using interval timing). Neither Levodopa nor DBS therapy led to significant improvements in timing abilities. Levodopa resulted in a strong trend towards impairing timing processes and caused a deterioration in perceptual coherency according to Weber’s Law. It is shown that timing abnormalities in PD occur in the seconds range but do not extend to the sub-second range. Furthermore, observed timing deficits were shown to not be solely caused by motor deficiency. This provides evidence to support internal clock models involving the BG (among other neural regions) in interval timing, and cerebellar control of sub-second timing. This study also revealed significant temporal perception deficits in recently diagnosed PD patients; thus, temporal perception abnormalities might act as an early disease marker, with the graphical tool showing potential for disease monitoring.

scholarly journals Event-Related Potentials Elicited by Face and Face Pareidolia in Parkinson’s Disease

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Gulsum Akdeniz ◽  
Gonul Vural ◽  
Sadiye Gumusyayla ◽  
Hesna Bektas ◽  
Orhan Deniz
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Visual Processing ◽  
Visual Recognition ◽  
Early Stage ◽  
Event Related Potentials ◽  
Control Group ◽  
Expression Recognition ◽  
Emotional Facial Expressions ◽  
Related Potentials

Background. Parkinson’s disease is associated with impaired ability to recognize emotional facial expressions. In addition to a visual processing disorder, a visual recognition disorder may be involved in these patients. Pareidolia is a type of complex visual illusion that permits the interpretation of a vague stimulus as something known to the observer. Parkinson’s patients experience pareidolic illusions. N170 and N250 waveforms are two event-related potentials (ERPs) involved in emotional facial expression recognition. Objective. In this study, we investigated how Parkinson’s patients process face and face-pareidolia stimuli at the neural level using N170, vertex positive potential (VPP), and N250 components of event-related potentials. Methods. To examine the response of face and face-pareidolia processing in Parkinson’s patients, we measured the N170, VPP, and N250 components of the event-related brain potentials in a group of 21 participants with Parkinson’s disease and 26 control participants. Results. We found that the latencies of N170 and VPP responses to both face and face-pareidolia stimuli were increased along with their amplitudes, and the amplitude of N250 responses decreased in Parkinson’s patients compared to the control group. In both control and Parkinson’s patients, face stimuli generated greater ERP amplitude and shorter latency in responses than did face-pareidolia stimuli. Conclusion. The results of our study showed that ERPs associated with face and also face-pareidolia stimuli processing are changed in early-stage neurophysiological activity in the temporoparietal cortex of Parkinson’s patients.

scholarly journals Glucosylceramide in cerebrospinal fluid of patients with GBA-associated and idiopathic Parkinson’s disease enrolled in PPMI

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Young Eun Huh ◽  
Hyejung Park ◽  
Ming Sum Ruby Chiang ◽  
Idil Tuncali ◽  
Ganqiang Liu ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cerebrospinal Fluid ◽  
De Novo ◽  
Early Stage ◽  
Rapid Decline ◽  
Healthy Controls ◽  
Protein Coding ◽  
Assessment Scores ◽  
Liquid Chromatography Tandem Mass

AbstractProtein-coding variants in the GBA gene modulate susceptibility and progression in ~10% of patients with Parkinson’s disease (PD). GBA encodes the β-glucocerebrosidase enzyme that hydrolyzes glucosylceramide. We hypothesized that GBA mutations will lead to glucosylceramide accumulation in cerebrospinal fluid (CSF). Glucosylceramide, ceramide, sphingomyelin, and lactosylceramide levels were measured by liquid chromatography-tandem mass spectrometry in CSF of 411 participants from the Parkinson’s Progression Markers Initiative (PPMI) cohort, including early stage, de novo PD patients with abnormal dopamine transporter neuroimaging and healthy controls. Forty-four PD patients carried protein-coding GBA variants (GBA-PD) and 227 carried wild-type alleles (idiopathic PD). The glucosylceramide fraction was increased (P = 0.0001), and the sphingomyelin fraction (a downstream metabolite) was reduced (P = 0.0001) in CSF of GBA-PD patients compared to healthy controls. The ceramide fraction was unchanged, and lactosylceramide was below detection limits. We then used the ratio of glucosylceramide to sphingomyelin (the GlcCer/SM ratio) to explore whether these two sphingolipid fractions altered in GBA-PD were useful for stratifying idiopathic PD patients. Idiopathic PD patients in the top quartile of GlcCer/SM ratios at baseline showed a more rapid decline in Montreal Cognitive Assessment scores during longitudinal follow-up compared to those in the lowest quartile with a P-value of 0.036. The GlcCer/SM ratio was negatively associated with α-synuclein levels in CSF of PD patients. This study highlights glucosylceramide as a pathway biomarker for GBA-PD patients and the GlcCer/SM ratio as a potential stratification tool for clinical trials of idiopathic PD patients. Our sphingolipids data together with the clinical, imaging, omics, and genetic characterization of PPMI will contribute a useful resource for multi-modal biomarkers development.

scholarly journals The Hsc70 Disaggregation Machinery Removes Monomer Units Directly from α-Synuclein Fibril Ends

2020 ◽  
Author(s):  
Matthias M. Schneider ◽  
Saurabh Gautam ◽  
Therese W. Herling ◽  
Ewa Andrzejewska ◽  
Georg Krainer ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neurodegenerative Diseases ◽  
De Novo ◽  
Dissociation Constants ◽  
Cellular Protein ◽  
Alpha Synuclein ◽  
Amyloid Formation ◽  
Nucleotide Exchange ◽  
Wide Range

AbstractMolecular chaperones contribute to the maintenance of cellular protein homeostasis through a wide range of mechanisms, including the assistance of de novo protein folding, the rescue of misfolded proteins, and the prevention of amyloid formation. Chaperones of the Hsp70 family have a striking capability of disaggregating otherwise irreversible aggregate structures such as amyloid fibrils that accumulate during the development of neurodegenerative diseases. However, the mechanisms of this key emerging functionality remain largely unknown. Here, we bring together microfluidic measurements with kinetic analysis and show that that the Hsp70 protein heat chock complement Hsc70 together with its two co-chaperones DnaJB1 and the nucleotide exchange factor Apg2 is able to completely reverse the aggregation process of alpha-synuclein, associated with Parkinson’s disease, back to its soluble monomeric state. Moreover, we show that this reaction proceeds with first order kinetics in a process where monomer units are taken off directly from the fibril ends. Our results demonstrate that all components of the chaperone triad are essential for fibril disaggregation. Lastly, we quantify the interactions between the three chaperones as well as between the chaperones and the fibrils in solution, yielding both binding stoichiometries and dissociation constants. Crucially, we find that the stoichiometry of Hsc70 binding to fibrils suggests Hsc70 clustering at the fibril ends. Taken together, our results show that the mechanism of action of the Hsc70–DnaJB1–Apg2 chaperone system in disaggregating α-synuclein fibrils involves the removal of monomer units without any intermediate fragmentation steps. These findings are fundamental to our understanding of the suppression of amyloid proliferation early in life and the natural clearance mechanisms of fibrillar deposits in Parkinson’s disease, and inform on the possibilities and limitations of this strategy in the development of therapeutics against synucleinopathies and related neurodegenerative diseases.

Gene expression analysis in modeling Parkinson’s disease

2020 ◽  
pp. 103-104
Author(s):  
М.М. Руденок ◽  
А.Х. Алиева ◽  
А.А. Колачева ◽  
М.В. Угрюмов ◽  
П.А. Сломинский ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Early Stage ◽  
Systemic Disease ◽  
Molecular Genetic ◽  
Presymptomatic Stage ◽  
Whole Transcriptome Analysis ◽  
Whole Transcriptome ◽  
The Brain ◽  
Transcriptome Level

Несмотря на очевидный прогресс, достигнутый в изучении молекулярно-генетических факторов и механизмов патогенеза болезни Паркинсона (БП), в настоящее время стало ясно, что нарушения в структуре ДНК не описывают весь спектр патологических изменений, наблюдаемых при развитии заболевания. В настоящее время показано, что существенное влияние на патогенез БП могут оказывать изменения на уровне транскриптома. В работе были использованы мышиные модели досимптомной стадии БП, поздней досимптомной и ранней симптомной (РСС) стадиями БП. Для полнотранскриптомного анализа пулов РНК тканей черной субстанции и стриатума мозга мышей использовались микрочипы MouseRef-8 v2.0 Expression BeadChip Kit («Illumina», США). Полученные данные указывают на последовательное вовлечение транскриптома в патогенез БП, а также на то, что изменения на транскриптомном уровне процессов транспорта и митохондриального биогенеза могут играть важную роль в нейродегенерации при БП уже на самых ранних этапах. Parkinson’s disease (PD) is a complex systemic disease, mainly associated with the death of dopaminergic neurons. Despite the obvious progress made in the study of molecular genetic factors and mechanisms of PD pathogenesis, it has now become clear that violations in the DNA structure do not describe the entire spectrum of pathological changes observed during the development of the disease. It has now been shown that changes at the transcriptome level can have a significant effect on the pathogenesis of PD. The authors used models of the presymptomatic stage of PD with mice decapitation after 6 hours (6 h-PSS), presymptomatic stage with decapitation after 24 hours (24 h-PSS), advanced presymptomatic (Adv-PSS) and early symptomatic (ESS) stages of PD. For whole transcriptome analysis of RNA pools of the substantia nigra and mouse striatum, the MouseRef-8 v2.0 Expression BeadChip Kit microchips (Illumina, USA) were used. As a result of the analysis of whole transcriptome data, it was shown that, there are a greater number of statistically significant changes in the tissues of the brain and peripheral blood of mice with Adv-PSS and ESS models of PD compared to 6 h-PSS and 24 h-PSS models. In general, the obtained data indicate the sequential involvement of the transcriptome in the pathogenesis of PD, as well as the fact that changes at the transcriptome level of the processes of transport and mitochondrial biogenesis can play an important role in neurodegeneration in PD at an early stage.

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