Ultrastructural immunocytochemical Synapse Changes In A Rat Model Of Parkinson’s Disease

1999 ◽  
Vol 5 (S2) ◽  
pp. 1230-1231
Author(s):  
C.K. Meshul ◽  
C. Allen ◽  
T. S. Kay
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dopamine Neurons ◽  
Current Therapy ◽  
Nerve Terminals ◽  
Glutamatergic Synapses ◽  
Excitatory Neurotransmitter ◽  
Neurotransmitter Glutamate ◽  
Progressive Disorder ◽  
The Brain

Parkinson's disease is a progressive disorder that is characterized by degeneration of the dopamine containing neurons located within the midbrain (substantia nigra). There is also substantial loss of dopamine within nerve terminals located within the striatum which originate from those dopamine neurons. Current therapy involves administration of the precursor to dopamine, namely l-dopa. This chemical is taken up into the brain and then converted to dopamine. Although replacement of dopamine is effective over the first few years, other movement disorders are associated with longterm l-dopa therapy. The l-dopa induced dyskinesias limit the usefulness of this type of therapy.Although loss of dopamine is the major neurochemical deficit in Parkinson's disease, other neurotransmitters within the striatum may also be altered. There is a major axonal projection from the cortex to the striatum. The corticostriatal pathway uses the excitatory neurotransmitter, glutamate, and dopamine is known to modulate the activity of glutamatergic synapses

Brain Grafting as a Treatment for Parkinson's Disease

Neurosurgery ◽  
1987 ◽  
Vol 20 (2) ◽  
pp. 335-342 ◽  
Author(s):  
Mark J. Perlow
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Clinical Manifestations ◽  
Dopamine Neurons ◽  
Clinical Aspects ◽  
Pathological Changes ◽  
Pharmacological Treatments ◽  
The Central Nervous System ◽  
The Brain

Abstract Parkinson's disease is an illness with neuropathological and neuroanatomical abnormalities in many areas of the central nervous system. Some clinical manifestations of this illness are correlated with pathological changes in the substantia nigra and with a loss of dopamine in the nigra and striatum. The most effective pharmacological treatments have used agents that either replace the lost dopamine or act as agonists on dopamine receptors. Recent studies in animal models of Parkinson's disease demonstrate that the loss of dopamine and many clinical manifestations of dopamine reduction can be reversed by transplantation of fetal dopamine-containing cells to specific dopamine-depleted areas of the brain. Long term viability of these transplants has also been demonstrated. The author suggests that the transplantation of dopamine neurons, even across species barriers, is a reasonable consideration for the treatment of human Parkinson's disease. This article reviews in detail the results of recent experiments and how the experience in these models might be utilized in determining a transplantation strategy for the treatment of specific clinical aspects of this illness.

scholarly journals Neuroregeneration in Parkinson’s Disease: From Proteins to Small Molecules

2019 ◽  
Vol 17 (3) ◽  
pp. 268-287 ◽  
Author(s):  
Yulia A. Sidorova ◽  
Konstantin P. Volcho ◽  
Nariman F. Salakhutdinov
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Small Molecules ◽  
Neurodegenerative Disorder ◽  
Dopamine Neurons ◽  
Current Therapy ◽  
Small Molecular Weight ◽  
Diagnostic Symptoms ◽  
Nigrostriatal Dopamine Neurons

Background: Parkinson’s disease (PD) is the second most common neurodegenerative disorder worldwide, the lifetime risk of developing this disease is 1.5%. Motor diagnostic symptoms of PD are caused by degeneration of nigrostriatal dopamine neurons. There is no cure for PD and current therapy is limited to supportive care that partially alleviates disease signs and symptoms. As diagnostic symptoms of PD result from progressive degeneration of dopamine neurons, drugs restoring these neurons may significantly improve treatment of PD. </P><P> Method: A literature search was performed using the PubMed, Web of Science and Scopus databases to discuss the progress achieved in the development of neuroregenerative agents for PD. Papers published before early 2018 were taken into account. </P><P> Results: Here, we review several groups of potential agents capable of protecting and restoring dopamine neurons in cultures or animal models of PD including neurotrophic factors and small molecular weight compounds. </P><P> Conclusion: Despite the promising results of in vitro and in vivo experiments, none of the found agents have yet shown conclusive neurorestorative properties in PD patients. Meanwhile, a few promising biologicals and small molecules have been identified. Their further clinical development can eventually give rise to disease-modifying drugs for PD. Thus, intensive research in the field is justified.

Fractionally delineate the neuroprotective function of calbindin-D28k in Parkinson’s disease

2018 ◽  
Vol 11 (08) ◽  
pp. 1850103 ◽  
Author(s):  
Hardik Joshi ◽  
Brajesh Kumar Jha
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dimensional Space ◽  
Cytosolic Calcium ◽  
The Body ◽  
Dopamine Neurons ◽  
Reaction Diffusion Equation ◽  
Substantia Nigra Pars Compacta ◽  
Brain Disorder ◽  
The Brain

Neuron is a fundamental unit of the brain, which is specialized to transmit information throughout the body through electrical and chemical signals. Calcium ([Formula: see text]) ions are known as second messengers which play important roles in the movement of the neurotransmitter. Calbindin-[Formula: see text] is a [Formula: see text] binding protein which is involved in regulation of intracellular [Formula: see text] ions and maintains [Formula: see text] homeostasis level, it also alters the cytosolic calcium concentration ([[Formula: see text]]) in nerve cells to keep the cell alive. Parkinson’s disease (PD) is a chronic progressive neurodegenerative brain disorder of the nervous system. Several regions of the brain indicate the hallmark of the PD. The symptoms of PD are plainly linked with the degeneration and death of dopamine neurons in the substantia nigra pars compacta located in midbrain which is accompanied by depletion in calbindin-[Formula: see text]. In the present paper, the neuroprotective role of calbindin-[Formula: see text] in the cytoplasmic [[Formula: see text]] distribution is studied. The elicitation in [[Formula: see text]] is due to the presence of low amount of calbindin-[Formula: see text] which can be portrayed and is a hallmark of PD. A one-dimensional space time fractional reaction diffusion equation is designed by keeping in mind the physiological condition taking place inside Parkinson’s brain. Computational results are performed in MATLAB.

scholarly journals An Introspective Approach: A Lifetime of Parkinson’s Disease Research and Not Much to Show for it Yet?

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 513
Author(s):  
Gordon W. Arbuthnott
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Death ◽  
Disease Progression ◽  
Dopamine Neurons ◽  
Motor Systems ◽  
Disease Research ◽  
Human Neuron ◽  
The Brain

I feel part of a massive effort to understand what is wrong with motor systems in the brain relating to Parkinson’s disease. Today, the symptoms of the disease can be modified slightly, but dopamine neurons still die; the disease progression continues inexorably. Maybe the next research phase will bring the power of modern genetics to bear on halting, or better, preventing cell death. The arrival of accessible human neuron assemblies in organoids perhaps will provide a better access to the processes underlying neuronal demise.

scholarly journals A Novel Small Molecule Supports the Survival of Cultured Dopamine Neurons and May Restore the Dopaminergic Innervation of the Brain in the MPTP Mouse Model of Parkinson’s Disease

2019 ◽  
Vol 10 (10) ◽  
pp. 4337-4349 ◽  
Author(s):  
Oleg V. Ardashov ◽  
Alla V. Pavlova ◽  
Arun Kumar Mahato ◽  
Yulia Sidorova ◽  
Ekaterina A. Morozova ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mouse Model ◽  
Small Molecule ◽  
Dopamine Neurons ◽  
The Brain

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.

Liposomes: Novel Drug Delivery Approach for Targeting Parkinson’s Disease

2020 ◽  
Vol 26 (37) ◽  
pp. 4721-4737 ◽  
Author(s):  
Bhumika Kumar ◽  
Mukesh Pandey ◽  
Faheem H. Pottoo ◽  
Faizana Fayaz ◽  
Anjali Sharma ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Drug Delivery ◽  
Parkinson's Disease ◽  
Side Effects ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Brain Targeting ◽  
Neural Cells ◽  
Blood Brain ◽  
The Brain

Parkinson’s disease is one of the most severe progressive neurodegenerative disorders, having a mortifying effect on the health of millions of people around the globe. The neural cells producing dopamine in the substantia nigra of the brain die out. This leads to symptoms like hypokinesia, rigidity, bradykinesia, and rest tremor. Parkinsonism cannot be cured, but the symptoms can be reduced with the intervention of medicinal drugs, surgical treatments, and physical therapies. Delivering drugs to the brain for treating Parkinson’s disease is very challenging. The blood-brain barrier acts as a highly selective semi-permeable barrier, which refrains the drug from reaching the brain. Conventional drug delivery systems used for Parkinson’s disease do not readily cross the blood barrier and further lead to several side-effects. Recent advancements in drug delivery technologies have facilitated drug delivery to the brain without flooding the bloodstream and by directly targeting the neurons. In the era of Nanotherapeutics, liposomes are an efficient drug delivery option for brain targeting. Liposomes facilitate the passage of drugs across the blood-brain barrier, enhances the efficacy of the drugs, and minimize the side effects related to it. The review aims at providing a broad updated view of the liposomes, which can be used for targeting Parkinson’s disease.

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