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Related Concept Videos

Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...
Parkinson Disease l: Introduction01:24

Parkinson Disease l: Introduction

Parkinson’s disease is a chronic, progressive neurodegenerative disorder that primarily affects movement. It is characterized by motor symptoms such as resting tremors, muscle rigidity, bradykinesia (slowness of movement), and postural instability. Patients may notice hand tremors at rest, stiffness during movement, or a shuffling gait. In addition to motor features, non-motor symptoms include sleep disturbances, mood and behavioral changes, constipation, and cognitive impairment, all of which...
Parkinson's Disease: Overview01:15

Parkinson's Disease: Overview

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 to...
Lysosomal Hydrolases01:22

Lysosomal Hydrolases

Lysosomes are the site for the degradation of macromolecules and biological polymers released during membrane trafficking events such as secretory, endocytic, autophagic, and phagocytic pathways. The membrane-enclosed area of the lysosome, called the lumen, contains hydrolytic enzymes active in an acidic environment. These acid hydrolases are functional at a pH between 4.5 and 5 and are involved in cellular processes such as cell signaling, energy metabolism, restoration of the plasma membrane,...
Neural Regulation01:37

Neural Regulation

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.
Parkinson's Disease: Treatment01:24

Parkinson's Disease: Treatment

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 its...

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Related Experiment Video

Updated: May 18, 2026

Assaying the Kinase Activity of LRRK2 in vitro
06:09

Assaying the Kinase Activity of LRRK2 in vitro

Published on: January 18, 2012

Presynaptic dysfunction in Parkinson's disease: a focus on LRRK2.

Elisa Belluzzi1, Elisa Greggio, Giovanni Piccoli

  • 1Department of Biology, University of Padova, Via Ugo Bassi 58/B, Padua, Italy.

Biochemical Society Transactions
|September 20, 2012
PubMed
Summary

Parkinson's disease (PD) involves synaptic dysfunction, particularly at the presynaptic neuron. Targeting presynaptic LRRK2 (leucine-rich repeat kinase 2) may offer early diagnostic and therapeutic strategies for PD.

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Rab10 Phosphorylation Detection by LRRK2 Activity Using SDS-PAGE with a Phosphate-binding Tag
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Rab10 Phosphorylation Detection by LRRK2 Activity Using SDS-PAGE with a Phosphate-binding Tag

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Human Peripheral Blood Neutrophil Isolation for Interrogating the Parkinson's Associated LRRK2 Kinase Pathway by Assessing Rab10 Phosphorylation
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Human Peripheral Blood Neutrophil Isolation for Interrogating the Parkinson's Associated LRRK2 Kinase Pathway by Assessing Rab10 Phosphorylation

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Last Updated: May 18, 2026

Assaying the Kinase Activity of LRRK2 in vitro
06:09

Assaying the Kinase Activity of LRRK2 in vitro

Published on: January 18, 2012

Rab10 Phosphorylation Detection by LRRK2 Activity Using SDS-PAGE with a Phosphate-binding Tag
08:55

Rab10 Phosphorylation Detection by LRRK2 Activity Using SDS-PAGE with a Phosphate-binding Tag

Published on: December 14, 2017

Human Peripheral Blood Neutrophil Isolation for Interrogating the Parkinson's Associated LRRK2 Kinase Pathway by Assessing Rab10 Phosphorylation
12:49

Human Peripheral Blood Neutrophil Isolation for Interrogating the Parkinson's Associated LRRK2 Kinase Pathway by Assessing Rab10 Phosphorylation

Published on: March 21, 2020

Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Parkinson's disease (PD) is a neurodegenerative disorder characterized by motor symptoms like bradykinesia and tremor.
  • Synaptic dysfunction is increasingly recognized as a critical factor in PD pathogenesis.
  • Many genes associated with PD have critical roles at the presynaptic site.

Purpose of the Study:

  • To investigate the presynaptic function of leucine-rich repeat kinase 2 (LRRK2) in Parkinson's disease.
  • To explore the role of LRRK2 mutations in synaptic dysfunction and neurotransmission defects in PD.
  • To evaluate the presynaptic site as a potential target for early PD diagnosis and therapy.

Main Methods:

  • Review of existing literature on LRRK2 mutations and their impact on presynaptic function in PD.
  • Analysis of studies on animal models of LRRK2 mutations focusing on neurotransmission and dopamine.
  • Examination of findings related to dopamine turnover in presymptomatic LRRK2-linked PD patients.

Main Results:

  • Mutations in LRRK2 are a major genetic cause of familial Parkinson's disease.
  • LRRK2 mutations are associated with defects in presynaptic vesicle trafficking and neurotransmission.
  • Altered dopamine flow and presynaptic plasticity are observed in LRRK2 PD models.
  • Impaired dopamine turnover is evident even in presymptomatic individuals with LRRK2 mutations.

Conclusions:

  • The presynaptic neuron is a key site for molecular defects in Parkinson's disease.
  • LRRK2 plays a critical role in presynaptic function and its dysfunction contributes to PD.
  • The presynaptic site, particularly involving LRRK2, represents a promising target for early diagnostic and therapeutic interventions in Parkinson's disease.