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This title is printed to order. This book may have been self-published. If so, we cannot guarantee the quality of the content. In the main most books will have gone through the editing process however some may not. We therefore suggest that you be aware of this before ordering this book. If in doubt check either the author or publisher’s details as we are unable to accept any returns unless they are faulty. Please contact us if you have any questions.
Parkinson's disease (PD) is a common neurodegenerative disorder affecting over 10 million people worldwide, with prevalence rising with age. It is characterized by motor symptoms like bradykinesia and rigidity, and non-motor symptoms driven by dopaminergic neuron loss in the substantia nigra pars compacta (SNpc). Key pathological features include alpha-synuclein aggregation into Lewy bodies, mitochondrial dysfunction, oxidative stress, and neuroinflammation.As PD progresses, dopamine depletion worsens, leading to advanced motor complications and non-motor impairments. Current treatments alleviate symptoms but do not prevent neurodegeneration. Understanding the mechanisms of alpha-synuclein aggregation, mitochondrial dysfunction, and neuroinflammation is essential for developing effective disease-modifying therapies.
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This title is printed to order. This book may have been self-published. If so, we cannot guarantee the quality of the content. In the main most books will have gone through the editing process however some may not. We therefore suggest that you be aware of this before ordering this book. If in doubt check either the author or publisher’s details as we are unable to accept any returns unless they are faulty. Please contact us if you have any questions.
Parkinson's disease (PD) is a common neurodegenerative disorder affecting over 10 million people worldwide, with prevalence rising with age. It is characterized by motor symptoms like bradykinesia and rigidity, and non-motor symptoms driven by dopaminergic neuron loss in the substantia nigra pars compacta (SNpc). Key pathological features include alpha-synuclein aggregation into Lewy bodies, mitochondrial dysfunction, oxidative stress, and neuroinflammation.As PD progresses, dopamine depletion worsens, leading to advanced motor complications and non-motor impairments. Current treatments alleviate symptoms but do not prevent neurodegeneration. Understanding the mechanisms of alpha-synuclein aggregation, mitochondrial dysfunction, and neuroinflammation is essential for developing effective disease-modifying therapies.