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Expert Definition

Understanding This Symptom

Medical Definition

Subject Matter Expert Verified

Parkinson's Disease is a progressive neurodegenerative disorder characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to dopamine deficiency in the basal ganglia.

This results in the cardinal motor features of tremor, bradykinesia, rigidity, and postural instability, along with non-motor symptoms including cognitive impairment, autonomic dysfunction, and psychiatric manifestations.

Quick Facts

Expert-reviewed by medical professionals
Based on current medical research
Updated for 2026 standards

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Healthy State

What Optimal Health Looks Like

Understanding how your body functions when healthy helps identify dysfunction

In a healthy dopaminergic system: (1) Substantia nigra neurons - dopaminergic neurons in the substantia nigra pars compacta produce and store dopamine in synaptic vesicles, maintaining stable population for motor control; (2) Basal ganglia function - the nigrostriatal pathway properly regulates movement initiation and inhibition through balanced dopamine signaling to the striatum (caudate and putamen); (3) Motor cortex coordination - the thalamocortical circuits receive appropriate dopaminergic input enabling smooth, coordinated voluntary movements; (4) Autonomic regulation - normal sympathetic and parasympathetic function maintains blood pressure, heart rate, and digestion; (5) Cognitive function - dopaminergic pathways to the prefrontal cortex support executive function, working memory, and attention; (6) Sleep architecture - normal REM and non-REM sleep cycles without fragmentation.

Healthy Function

Your body is designed to maintain balance and self-regulate

Optimal Range
Development Process

How This Develops

1

Alpha-synuclein pathology - misfolded alpha-synuclein protein aggregates into Lewy bodies within dopaminergic neurons, causing cellular dysfunction and death in the substantia nigra; (

2

Mitochondrial dysfunction - complex I deficiency in dopaminergic neurons leads to ATP depletion, increased reactive oxygen species, and neuronal apoptosis; (

3

Neuroinflammation - activated microglia release pro-inflammatory cytokines (IL-

4

that damage dopaminergic neurons; (

5

Oxidative stress - dopamine metabolism via MAO-B produces hydrogen peroxide, and reduced glutathione levels impair antioxidant defenses in dopaminergic neurons; (

6

Ubiquitin-proteasome system impairment - failure to degrade misfolded proteins leads to toxic protein accumulation; (

7

Neurotrophic factor deficiency - reduced BDNF (brain-derived neurotrophic factor) impairs neuronal survival and plasticity; (

8

Glial cell dysfunction - astroglial and microglial dysfunction fails to support neuronal health and clear toxic proteins; (

9

Spreading pathology - prion-like propagation of alpha-synuclein aggregates explains the progressive spread from brainstem to cortical regions

Understanding the mechanism helps us target the root cause rather than just treating symptoms.

Cost of Waiting

What Happens If Left Untreated

Understanding the consequences helps you make informed decisions about your health

Short-Term Consequences

Days to weeks

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Time Matters

Don't wait for symptoms to worsen. Early intervention leads to better outcomes.

Common Questions

Frequently Asked Questions

Expertise Behind This Guide

Evidence-Based Information

Dr. Hafeel Afsar, DHA Licensed Integrative Medicine

References & Further Reading

Kalia LV et al. 'Parkinson's disease.' Lancet. 2015;386(9996):896-912. PMID: 25904081
Poewe W et al. 'Parkinson disease.' Nat Rev Dis Primers. 2017;3:17013. PMID: 28332488
Jankovic J et al. 'Parkinson disease: Clinical features and pathogenesis.' Nat Rev Neurol. 2023;19(11):659-673. PMID: 37845204

This information is for educational purposes and not a substitute for professional medical advice.