Systemic Amyloidoses

Ramı́rez-Alvarado, Marina; Buxbaum, Joel N.

doi:10.1002/9780470572702.ch15

Cited by 2 publications

(3 citation statements)

References 69 publications

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“…Its symptoms include motoric abnormalities due to dopamine deficits in the striatum resulting in resting tremor, stiffness and slow movements, in addition to non-dopaminergic related symptoms of dementia and depression, anxiety and autonomic dysfunction [2, 3]. Approximately 85–90% of PD cases are sporadic, i.e.…”

Section: Parkinson's Disease Overviewmentioning

confidence: 99%

“…Five to fifteen percent of PD patients have monogentically-inherited forms of the disease that are associated with one of the six identified genes. Of these genes, mutations in SNCA (PARK1 – 4) and LRRK2 ( PARK8 ) are responsible for autosomal-dominant PD forms, while Parkin (PARK2) , DJ-1 (PARK7) , ATP13A2 (PARK9) , PTEN-induced putative kinase 1 ( PINK1) , and leucine-rich repeat kinase 2, LRRK2 (PARK8) account for autosomal recessive mode of inheritance of PD [3, 12, 13]. These mutations exacerbate neurodegenerative mechanisms, such as protein aggregation, oxidative stress and impaired protein degradation that contribute to PD pathogenesis.…”

Section: Parkinson's Disease Overviewmentioning

confidence: 99%

“…However, other studies have suggested otherwise. For example, it has been revealed that alpha-synuclein self-assembles into proto-fibrils and fibrils and aggregates to form insoluble amyloid fibrils composing Lewy bodies and neurites in the brain that may by cytotoxic [1, 3]. These aggregates are thought to contribute to PD symptomology by disrupting cellular homeostasis and causing neuron death through their toxic effects on neighboring cells and synapses [24].…”

Section: Genetic Factorsmentioning

confidence: 99%

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Disease-Toxicant Interactions in Parkinson’s Disease Neuropathology

2016

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Human disease commonly manifests as a result of complex genetic and environmental interactions. In the case of neurodegenerative diseases, such as Parkinson's disease (PD), understanding how environmental exposures collude with genetic polymorphisms in the central nervous system (CNS) to cause dysfunction is critical in order to develop better treatment strategies, therapies, and a more cohesive paradigm for future research. The intersection of genetics and the environment in disease etiology is particularly relevant in the context of their shared pathophysiological mechanisms. This review offers an integrated view of disease-toxicant interactions in PD. Particular attention is dedicated to how mutations in the genes SNCA, parkin, leucine-rich repeat kinase 2 (LRRK2) and DJ-1, as well as dysfunction of the ubiquitin proteasome system, may contribute to PD and how exposure to heavy metals, pesticides and illicit drugs may further the consequences of these mutations to exacerbate PD and PD-like disorders. Although the toxic effects induced by exposure to these environmental factors may not be the primary causes of PD, their mechanisms of action are critical for our current understanding of the neuropathologies driving PD. Elucidating how environment and genetics collude to cause pathogenesis of PD will facilitate the development of more effective treatments for the disease. Additionally, we discuss the neuroprotection exerted by estrogen and other compounds that may prevent PD and provide an overview of current treatment strategies and therapies.

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Section: Parkinson's Disease Overviewmentioning

confidence: 99%

Section: Parkinson's Disease Overviewmentioning

confidence: 99%

Section: Genetic Factorsmentioning

confidence: 99%

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Disease-Toxicant Interactions in Parkinson’s Disease Neuropathology

2016

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A Perspective on Interdicting in Protein Misfolding for Therapeutic Drug Design: Modulating the Formation of Nonlocal Contacts in α-Synuclein as a Strategy against Parkinson’s Disease

Bergasa-Caceres,

Rabitz

2024

J. Phys. Chem. B

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In recent work we proposed that interdiction in the earliest contact-formation events along the folding pathway of key viral proteins could provide a novel avenue for therapeutic drug design. In this Perspective we explore the potential applicability of the protein folding interdiction strategy in the realm of neurodegenerative diseases with a specific focus on synucleinopathies. In order to fulfill this goal we review the interdiction proposal and its practical challenges, and we present new results concerning design strategies for possible peptide drugs that could be useful in preventing α-synuclein aggregation.

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Systemic Amyloidoses

Cited by 2 publications

References 69 publications

Disease-Toxicant Interactions in Parkinson’s Disease Neuropathology

Disease-Toxicant Interactions in Parkinson’s Disease Neuropathology

A Perspective on Interdicting in Protein Misfolding for Therapeutic Drug Design: Modulating the Formation of Nonlocal Contacts in α-Synuclein as a Strategy against Parkinson’s Disease

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