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Author: Mary Ann Chapman

A Closer Look at Lewy Bodies

A Closer Look at Lewy Bodies

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Since the early 1900s, Lewy bodies have been a primary distinguishing feature of Parkinson’s disease pathology. First described by Dr. Friederich Lewy in 1912, Lewy bodies appear under light microscopes as large sphere-shaped masses in neuronal cell bodies and are accompanied by spindle-like inclusions in neuronal process referred to as Lewy neurites.1 In addition to aggregated alpha synuclein and ubiquitin, Lewy bodies contain at least 90 other molecules.2 Lewy Bodies and Neurites Lewy bodies (round brown/black structures) and Lewy neurites…

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Do Neurons Die in Parkinson’s Disease Because They Lack Trophic Support?

Do Neurons Die in Parkinson’s Disease Because They Lack Trophic Support?

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Lipids are in the news again, with a recently published hypothesis proposing that age-dependent decreases in GM1 ganglioside can trigger Parkinson’s disease.(1) Forsayeth and Hadaczek describe parkinsonian-like neurodegeneration in humans and animals with mutations in ganglioside metabolic pathways. In their view, the age-related loss of GM1 prevents glial cell derived neurotrophic factor (GDNF) from signaling and, without this trophic support, selected catecholaminergic neurons die. Gangliosides are lipids that consist of carbohydrates with a 9-carbon backbone and a carboxylic acid group. They…

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Transplanted Cells in Parkinson’s Disease Continue to Inform

Transplanted Cells in Parkinson’s Disease Continue to Inform

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It’s been nearly a decade since groups in the United States1 and Sweden2 reported alpha synuclein pathology in transplanted cells grafted into the brains of people with Parkinson’s disease. The Lewy body-like inclusions were accompanied by other markers of neuronal dysfunction that apparently developed over 10+ years. The pathology is remarkable because the transplanted cells were young and genetically unrelated to the individuals with Parkinson’s disease, suggesting an ongoing degenerative process in the parkinsonian brain and the presence of a pathological…

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Parkinson’s Disease Genes Linked to Lipids

Parkinson’s Disease Genes Linked to Lipids

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There’s no shortage of genes associated with Parkinson’s disease. Known mutations in 6 genes can cause early onset or classical, late onset Parkinson’s disease, and mutations in at least 2 more can cause atypical parkinsonian syndromes.1 Additional genetic loci and identified genes increase the susceptibility to Parkinson’s disease. Although the identified genes are not all part of the same biological pathway, identifying commonalities among them may provide clues to the disease process.  One theme that emerges from these studies is…

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On the Trail of Olfactory Deficits in Parkinson’s Disease

On the Trail of Olfactory Deficits in Parkinson’s Disease

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A friend told me that his father could never smell cookies or coffee—a seemingly harmless idiosyncrasy that was frequently the subject of family jokes. No one had any idea that the olfactory deficits could be linked to Parkinson’s disease, and everyone was surprised by the diagnosis when motor symptoms appeared years later.

From Glucocerebrosidase to Autophagy and Mitophagy in Parkinson’s Disease

From Glucocerebrosidase to Autophagy and Mitophagy in Parkinson’s Disease

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Over the past two decades, researchers have documented numerous links between Parkinson’s disease and Gaucher disease. Rare patients with Gaucher disease show parkinsonian symptoms1 and many more have family members with Parkinson’s disease.2 Lewy bodies—large aggregates of alpha synuclein protein characteristic of Parkinson’s disease—have been identified in the brains of Gaucher patients,3 and approximately 5-10% of those with sporadic Parkinson’s disease show mutations in the glucocerebrosidase gene, the cause of Gaucher disease.4,5

Following the Pathway Analysis in Parkinson’s Disease

Following the Pathway Analysis in Parkinson’s Disease

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Pathway analyses of genomic data make intuitive sense to me for conditions like Parkinson’s disease. Only a handful of single genes have been consistently associated with Parkinson’s, but the genomic picture is certainly larger, and we are faced with the complex possibility that numerous rarer variations play a role. The underlying assumption of pathway analyses is that diverse genomic variations may be part of common pathways that, when dysfunctional, may lead to disease.

Rationale for Nilotinib and Other Kinase Inhibitors in Parkinson’s Disease

Rationale for Nilotinib and Other Kinase Inhibitors in Parkinson’s Disease

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For many months, those who follow Parkinson’s disease clinical research have been anticipating the results of a small study of the cancer drug nilotinib. The study, now published in Journal of Parkinson’s Disease,1 suggests that nilotinib and perhaps other kinase inhibitors are worthy of more serious attention as treatments for Parkinson’s and related diseases. The “related diseases” part is important here because 5 of the 12 study participants were diagnosed with dementia with Lewy bodies.

Synaptic Dysfunction in Parkinson’s Disease: The Chicken or the Egg?

Synaptic Dysfunction in Parkinson’s Disease: The Chicken or the Egg?

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Figuring out what happens first in Parkinson’s disease is a difficult task. People are not usually diagnosed until they experience motor symptoms, at which point 70-80% of their nigrostriatal dopamine neurons have already died. This makes it hard to trace the sequence of events that leads to neuronal degeneration.

Why Don’t We All Get Parkinson’s Disease?

Why Don’t We All Get Parkinson’s Disease?

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This seems like an odd question given that only a small percentage of people actually get Parkinson’s disease. Nevertheless, the question has always perplexed me. Here’s my rationale. The main neurons responsible for the motor symptoms of Parkinson’s disease are dopamine-containing cells that project from the substantia nigra pars compacta to the striatum. In the striatum, each nigrostriatal dopamine neuron branches into a dizzying array of tiny appendages that make hundreds of thousands of synapses.1, 2 And these neurons do…

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