Blog Posts

New data supports connection between mitochondrial CYP2D6 activation of chemicals to toxic intermediates and Parkinson's disease risk

6/23/2019

A new study by Narayan Avadhani and Mrittika Chattopadhyay, published in the Journal of Biological Chemistry, suggests that the enzyme, mitochondrial cytochrome P4502D6, plays a role in Parkinson's disease.

Previous studies have implicated MPTP and similar toxic compounds in Parkinson's disease risk. Earlier work by Avadhani and colleagues has shown that CYP2D6 plays a role in metabolizing MPTP to the toxic metabolite MPP. The results of their new study indicate that toxicants resembling MPTP found in tobacco smoke, alcohol, and some foods are also activated by CYP2D6. This route of metabolic activation was shown in a mouse model, to result in neuronal damage and oxidative stress, and symptoms akin to Parkinson's. "CYP2D6 is known to play a role in influencing the activity of a number of drugs," said Avadhani.

To learn more about the connection between neurotoxicant metabolism and PD risk and age at onset of this disease read my review on the topic here.

Link to original news story here

Link to article in JBC

Persons Diagnosed with Bipolar Disorder Develop Parkinson's Disease Younger

5/24/2019

Maureen Salamon from WebMD is reporting on the results of a new study indicating that patients younger than age 65 years old who have previously been diagnosed with bipolar disorder are at an increased risk for developing Parkinson's disease. It is well recognized that many of the medications used to treat bipolar disorder can cause iatrogenic drug-induced parkinsonism suggesting that there may be a point of mechanistic interaction between these medications and age at onset of Parkinson's disease.

Link to story on WedMD

Link to original article in Neurology.

Chemotherapy accelerates age-related development of tauopathy in a rodent model of aging

4/10/2019

Tauopathy is neuropathological finding associated with Alzheimer's disease. A new study from a group of researchers at the MD Anderson Cancer Center suggests that the neurotoxic side effects of the chemotherapy agent cisplatin accelerates formation of Tau-1 clusters and decreases levels of the post-synaptic marker PSD95 and of the presynaptic marker synaptophysin in the hippocampus. These findings demonstrate for the first time that certain neurotoxic chemotherapy agents can accelerate development of tauopathy and loss of synaptic integrity in the hippocampus. This finding demonstrates how neurotoxic chemicals can modify the subclinical and clinical course of a neurodegenerative disease associated with memory dysfunction. These results are of importance to patients diagnosed with cancer who also have a family history of Alzheimer's disease. If you have any concerns about these findings please discuss these with your treating physician.

Link to publication

Link Between Manganese Exposure and Parkinson’s Disease Development Further Elucidated

3/19/2019

A new study by Harischandra and colleagues which appear in Science Signaling suggests that manganese promotes the aggregation and prion-like cell-to-cell exosomal transmission of α-synuclein which is implicated in Parkinson's disease. Welders exposed to manganese were found to have increased misfolded α-synuclein in their serum exosomes.

These novel findings shed light on a previously unrecognized mechanism via which manganese can exacerbate and unmask latent idiopathic Parkinson's disease.

Link to original peer reviewed publication

Exposure to Pesticides Implicated in Progression of ALS

3/1/2019

A study by Goutman and colleagues which appears in the Journal of Neurology Neurosurgery and Psychiatry finds that higher plasma levels of persistent environmental pollutants is a risk factor in the progression of ALS.

These findings indicate that environmental exposures to toxicants plays a role in the progression of neurodegenerative disease such as ALS.

Link to original news report in Science Daily

Link to publication

Nanoimaging Technology Sheds Light on how Manganese Contributes to the Development of Parkinsonism

2/10/2019

A new study by Carmona et al. (2019) suggests that a mutation in a gene (Slc30a10) implicated in familial forms of parkinsonism plays a role in the accumulation of manganese (Mn) within the golgi apparatus of cells. This gene encodes for a cell surface protein involved in the efflux of Mn which protects the cell against Mn toxicity. Mutations in this gene result in synthesis of a defective protein that does not does not function properly resulting in accumulation of Mn within the cell. Carmona and colleagues (2019) used a newly developed SXRF cryogenic nanoimaging technology to show that Mn gets trapped inside vesicles within the Golgi apparatus (see image below) suggesting that interactions between Mn and vesicular trafficking machinery may play a role in the parkinsonism.

Link to story in Physics World by Belle Dumé

Link to citation in PubMed

Welders have elevated serum levels of ASC and proinflammatory cytokines compared to age-matched controls.

1/11/2019

Results of a new study by Sarkar and colleagues (2019) published in the journal Science Signaling suggests that exposure to constituents of welding fumes amplifies NLRP3 inflammasome signaling and exosomal ASC release. The NLRP3 inflammasome oligomeric complex is composed of an adapter protein ASC (apoptosis- associated speck-like protein containing a CARD), caspase-1, and NLRP3. Welders have plasma exosomes that contain more of the adapter protein ASC (apoptosis- associated speck-like protein containing a CARD) than controls. Many factors have been implicated in activation of the NLRP3 inflammasome cascade including mitochondrial dysfunction which can be mediated by manganese. However, when these investigators analyzed whole blood for manganese levels in welders and unexposed controls they did not observe any significant differences. More work is needed to determine which constituents of welding fumes are are associated with these observations.

Link to publication

Heavy metals induce ALS-linked TDP-43 neuropathology

11/15/2018

Researchers from Boston University School of Medicine (Ash et al., 2019) have reported on new data demonstrating a direct mechanistic link between exposure to heavy metals and risk for developing ALS. These studies showed that lead (Pb) and methyl mercury (MeHg) disrupt the homeostasis of TDP-43 in neurons. These metals also triggered the accumulation of insoluble TDP-43 in cultured cells and in the cortices of exposed mice. These new data provide evidence for a mechanistic link between a commonly cited environmental risk factor for ALS, and molecular changes in TDP-43, the primary pathological protein accumulating in ALS.

Link to article

Manganese exposure exacerbates progressive motor deﬁcits and neurodegeneration in the Mito Park mouse model of Parkinson’s disease.

10/9/2018

A recently study by Langley and colleagues used the MitoPark mouse model of PD which recapitulates the behavioral symptoms and neuropathological changes associated with PD to investigate the effects of low level manganese exposure on disease progression. The study found that exposure to manganese (10 mg/kg, p.o. daily for 4 weeks) accelerated the rate of progression of motor deﬁcits in MitoPark mice and also enhanced oxidative damage in the striatum and substantia nigra (SN) of these mice. These new results provide additional data in the growing body of research indicating that neurotoxicants such as manganese that increase oxidative stress can augment mitochondrial dysfunction and exacerbate nigrostriatal neurodegeneration which in turn can unmask latent PD-related behavioral symptoms.

Link to citation in Pubmed

ADHD associated with increase risk of Parkinson's disease and similar disorders

9/13/2018

ScienceDaily is reporting on recent research from Glen Hanson and colleagues from the University of Utah showing that Attention Deficit Hyperactivity Disorder is associated with an increased risk for parkinsonism. The study found that patient's with ADHD were more likely to develop early onset parkinsonism than individuals of the same gender and age who did not have ADHD. The risk was dramatically increased, eight- to nine-fold among those ADHD patients who had a history of being treated with amphetamine-like drugs. This study adds to the growing body of literature implicating chemicals in a younger age at onset of Parkinson's disease and other forms of parkinsonism.

Link to story in ScienceDaily

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Dr. Marcia Ratner shares and reviews the news.

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Last updated: December 23, 2020

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Neurotoxicants.com is strictly an information and news website about the associations between chemical exposure and neurological disease. The information provided on this site is meant to complement and not replace any advice or information from your healthcare professional. This content is not intended to be a substitute for professional medical advice or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. While every care has been exercised in compiling and publishing the data contained in these pages, Neurotoxicants.com accepts no responsibility for errors or omissions to of the information provided on this website. Neurotoxicants.com cannot be held liable for typographical errors, layout error or misinformation contained herein. Copyright © 2015-2020, Dr. Marcia H. Ratner, DABT, Proprietor and Principal Consultant, D.B.A. Neurotoxicants.com is registered with Dun and Bradstreet. All Rights Reserved. Privately funded; Neurotoxicants.com does not accept or host paid advertising. Neurotoxicants.com does not accept payment from any external influences which could affect the objectivity of the editorial content of this website.

Updated December 23, 2020

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