Dietary fatty acids and the risk of Parkinson disease

Lau, Lonneke M. L. de; Bornebroek, M.; Witteman, Jacqueline C. M.; Hofman, Albert; Koudstaal, Peter J.; Breteler, Monique M.B.

doi:10.1212/01.wnl.0000166038.67153.9f

Cited by 237 publications

(165 citation statements)

References 47 publications

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“…Moreover, this study showed that switching MUFAs and PUFAs for saturated fats prevented the increase in cholesterol expected from intake of a high-fat diet ( 157 ). In a prospective study of older adults, increased consumption of total fats, MUFAs, and PUFAs was associated with a lower risk of PD ( 158 ).…”

Section: Pdmentioning

confidence: 66%

Ketogenic diets, mitochondria, and neurological diseases

Gano

Patel

Rho

2014

Journal of Lipid Research

217

193

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Section: Pdmentioning

confidence: 66%

Ketogenic diets, mitochondria, and neurological diseases

Gano

Patel

Rho

2014

Journal of Lipid Research

217

193

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“…All participating patients reported moderate to very good improvement in symptoms. Further, as in Alzheimer's disease, consumption of foods containing increased amounts of essential fatty acids has been associated with a lower risk of developing Parkinson's disease (de Lau et al, 2005).…”

Section: Parkinson's Diseasementioning

confidence: 99%

Neuroprotective and disease-modifying effects of the ketogenic diet

Gąsior¹,

Rogawski²,

Hartman³

2006

Behavioural Pharmacology

402

324

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The ketogenic diet has been in clinical use for over 80 years, primarily for the symptomatic treatment of epilepsy. A recent clinical study has raised the possibility that exposure to the ketogenic diet may confer long-lasting therapeutic benefits for patients with epilepsy. Moreover, there is evidence from uncontrolled clinical trials and studies in animal models that the ketogenic diet can provide symptomatic and disease-modifying activity in a broad range of neurodegenerative disorders including Alzheimer's disease and Parkinson's disease, and may also be protective in traumatic brain injury and stroke. These observations are supported by studies in animal models and isolated cells that show that ketone bodies, especially β-hydroxybutyrate, confer neuroprotection against diverse types of cellular injury. This review summarizes the experimental, epidemiological and clinical evidence indicating that the ketogenic diet could have beneficial effects in a broad range of brain disorders characterized by the death of neurons. Although the mechanisms are not yet well defined, it is plausible that neuroprotection results from enhanced neuronal energy reserves, which improve the ability of neurons to resist metabolic challenges, and possibly through other actions including antioxidant and anti-inflammatory effects. As the underlying mechanisms become better understood, it will be possible to develop alternative strategies that produce similar or even improved therapeutic effects without the need for exposure to an unpalatable and unhealthy, high-fat diet.

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“…The role that fat plays in PD is most likely related to the type of fat in the patient's diet (De Lau et al, 2005), the patient's HDL/LDL ratio, total cholesterol levels and genetic factors. Ideally, large prospective randomized controlled studies are needed to clarify the associations between fat intake and PD.…”

Section: Nutrients With a Questionable Role In Pd Fatmentioning

confidence: 99%

“…Because of the limited number of patients, the difficulty in adhering to a hyperketonemia diet, and the lack of healthy controls, the authors were not able to rule out a placebo effect. The promising results from this preliminary study suggest that another clinical trial of the ketogenic diet that includes a larger number of patients is warranted.Dietary intake of PUFAs and monounsaturated fatty acids (MUFAs) might influence the risk of PD (Abbott et al, 2003;De Lau et al, 2005). It has been reported in other disease models that PUFA's have anti-inflammatory and neuroprotective properties (Blok et al, 1996;Simopoulos, 1999;Youdim et al, 2000;Kim et al, 2001) and MUFAs are thought to reduce oxidative stress (Colette et al, 2003;Moreno and Mitjavila, 2003).…”

mentioning

confidence: 99%

Splice Variant Biomarkers for Parkinson's Disease

Potashkin¹

2014

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. REPORT DATEMay PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES) AND ADDRESS(ES) PERFORMING ORGANIZATION REPORT NUMBERRosalind Franklin U. Medicine & Science 3333 Green Bay Rd. North Chicago, IL 60064-3037 SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S) U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited SUPPLEMENTARY NOTES ABSTRACTRecently we identified splice variants in whole blood than can distinguish early stage Parkinson's disease (PD) patients from healthy and neurodegenerative controls. The proposed studies will test the hypothesis that the biomarkers will be useful for identifying individuals at risk for PD and for identifying signaling pathways that are disrupted in PD. We are testing the expression of the biomarkers in RNA prepared from whole blood of hyposmic participants in the Parkinson's Associated Risk Study (PARS) (Technical Objective 1.0). In order to establish a model for testing the function of the biomarkers, we are determining whether their expression is altered in human olfactory neurosphere-derived (hONS) cells derived from idiopathic PD patients and healthy controls (Technical Objective 2.0). To determine the signaling pathways affected in PD and identify additional biomarkers, we are using network analysis (Technical Objective 3.0). During year 1, RNA and cDNA was prepared from PARS samples from Year 0 (baseline) and Year 2. Quantitative polymerase chain reactions were initiated for two of the biomarkers (APP, HNF4α). Expression of the biomarkers was tested in hONS. We also developed network approaches to reveal the common molecular pathways involved with PD and type 2 diabetes (T2DM). Using these networks, we identified APP, HNF4A and SOD2 mRNAs as blood biomarkers predictive of early stage PD. In addition, we determined that HNF4A mRNA may be a progression marker in blood for PD. SUBJECT TERMSParkinson's disease, biomarkers, neurodegeneration, network and pathway analysis 12-15Santiago 16-23Sei...

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Dietary fatty acids and the risk of Parkinson disease

Abstract: These findings suggest that high intake of unsaturated fatty acids might protect against Parkinson disease.

Cited by 237 publications

References 47 publications

Ketogenic diets, mitochondria, and neurological diseases

Ketogenic diets, mitochondria, and neurological diseases

Neuroprotective and disease-modifying effects of the ketogenic diet

Splice Variant Biomarkers for Parkinson's Disease

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