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Related Concept Videos

Parkinson's Disease: Overview01:15

Parkinson's Disease: Overview

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Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is...
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Neuroplasticity01:01

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Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.
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Parkinson's Disease: Treatment01:24

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Neurodegenerative disorders, such as Parkinson's Disease (PD), involve the gradual and irreversible destruction of neurons in particular brain areas. These disorders exhibit standard features like proteinopathies, selective vulnerability of some neurons, and an interaction of intrinsic properties, genetics, and environmental influences in neural injury.
Parkinson's Disease is primarily a result of the loss of dopaminergic neurons in the substantia nigra pars compacta. The cornerstone of...
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Neural Regulation01:37

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Digestion begins with a cephalic phase that prepares the digestive system to receive food. When our brain processes visual or olfactory information about food, it triggers impulses in the cranial nerves innervating the salivary glands and stomach to prepare for food.
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EPS and iPS Cells in Disease Research01:21

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Embryonic and induced pluripotent stem cells are excellent models for disease research because of their ability to self-renew and differentiate into most cell types. Somatic cells from a patient are isolated and reprogrammed into induced pluripotent stem cells or iPSCs. These iPSCs are later differentiated into the desired cell type, which mirrors the diseased cell of the patient. In this way, disease models have been created for investigating diseases such as Down syndrome, type I diabetes,...
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Long-term Potentiation01:35

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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Related Experiment Video

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Murine Model for Parkinson's Disease: from 6-OH Dopamine Lesion to Behavioral Test
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Neuroplasticity in Parkinson's disease.

Bogdan Ovidiu Popescu1,2, Lucia Batzu3,4, Pedro J Garcia Ruiz5

  • 1Department of Clinical Neurosciences, 'Carol Davila' University of Medicine and Pharmacy Bucharest, Bucharest, Romania. bogdan.popescu@umfcd.ro.

Journal of Neural Transmission (Vienna, Austria : 1996)
|August 5, 2024
PubMed
Summary

Parkinson's disease (PD) involves brain changes at multiple levels. This review explores neuroplasticity in PD, examining beneficial and maladaptive responses to treatments and disease progression.

Keywords:
AMPABDNFBiomarkersDopamineNMDANeuroplasticityParkinson’s disease

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Area of Science:

  • Neuroscience
  • Neurology
  • Neurodegeneration

Background:

  • Parkinson's disease (PD) is a prevalent neurodegenerative disorder with increasing incidence.
  • While no cure exists, effective treatments are available for PD, even in advanced stages.
  • Neuroplasticity, the brain's adaptive capacity, is crucial for understanding PD pathology and treatment responses.

Purpose of the Study:

  • To review current knowledge on neuroplasticity in Parkinson's disease.
  • To examine neuroplastic changes at network, cellular, and molecular levels in PD.
  • To analyze both beneficial and detrimental neuroplastic responses in PD.

Main Methods:

  • Literature review of neuroplasticity in Parkinson's disease.
  • Analysis of neuroplasticity at network, cellular, and molecular levels.
  • Examination of adaptive and maladaptive neuroplasticity, including treatment effects.

Main Results:

  • Neuroplasticity in PD involves complex network, cellular, and molecular adaptations.
  • Beneficial neuroplastic effects include enhanced neuronal efficacy.
  • Maladaptive neuroplasticity, such as levodopa-induced dyskinesia, can occur.

Conclusions:

  • Understanding neuroplasticity is key to managing Parkinson's disease.
  • Physical activity and treatments can modulate neuroplasticity in PD.
  • Biomarker identification for neuroplasticity holds therapeutic potential.