scholarly journals Traumatic brain injury in the prodromal period of Parkinson's disease: A large epidemiological study using medicare data

2017 ◽  
Vol 82 (5) ◽  
pp. 744-754 ◽  
Author(s):  
Alejandra Camacho-Soto ◽  
Mark N. Warden ◽  
Susan Searles Nielsen ◽  
Amber Salter ◽  
David L. Brody ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Traumatic Brain Injury ◽  
Parkinson's Disease ◽  
Brain Injury ◽  
Epidemiological Study ◽  
Medicare Data

Caracole as a Potential Neuroprotective Agent for Neurological Diseases: A Systematic

2021 ◽  
Vol 20 ◽  
Author(s):  
Mohammad Zamanian ◽  
Małgorzata Kujawska ◽  
Marjan Nikbakht Zadeh ◽  
Amin Hassanshahi ◽  
Soudeh Ramezanpour ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Traumatic Brain Injury ◽  
Parkinson's Disease ◽  
Brain Injury ◽  
Neurological Diseases ◽  
Antioxidant Systems ◽  
Neuroprotective Agent ◽  
The Impact

Background & objective: Neurological diseases are becoming a significant problem worldwide, with the elderly at a higher risk of being affected. Several researchers have investigated the neuroprotective effects of Carvacrol (CAR) (5-isopropyl-2-methyl phenol). This review systematically surveys the existing literature on the impact of CAR when used as a neuroprotective agent in neurological diseases. Methods: The systematic review involved English articles published in the last ten years obtained from PubMed, Google Scholar, and Scopus databases. The following descriptors were used to search the literature: “Carvacrol” [Title] AND “neuroprotective (neuroprotection)” [Title] OR “stroke, traumatic brain injury, Alzheimer's disease, Parkinson's disease, seizure, epilepsy [Title]. Results: : A total of 208 articles were retrieved during the search process, but only 20 studies met the eligibility criteria and were included for review. A total of 20 articles were identified, in which the efficacy of CAR was described in experimental models of stroke, traumatic brain injury, Parkinson’s disease, Alzheimer’s disease, , epilepsy, and seizure, through motor deficits improvements in neurochemical activity, especially antioxidant systems, reducing inflammation, oxidative stress and apoptosis as well as inhibition of TRPC1 and TRPM7. Conclusion : The data presented in this study support the beneficial impact of CAR on behavioural and neurochemical deficits. CAR benefits accrue because of its anti-apoptotic, antioxidant, and anti-inflammatory properties. Therefore, CAR has emerged as an alternative treatment for neurological disorders based on its properties.

The impact of traumatic brain injury on cognitive and neuropsychiatric symptoms of Parkinson’s disease

2019 ◽  
Vol 32 (1) ◽  
pp. 46-60 ◽  
Author(s):  
Julie M. Joyce ◽  
Oury Monchi ◽  
Zahinoor Ismail ◽  
Mekale Kibreab ◽  
Jenelle Cheetham ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Traumatic Brain Injury ◽  
Parkinson's Disease ◽  
Brain Injury ◽  
Neuropsychiatric Symptoms ◽  
The Impact

Neurological Disorders of Attention

2014 ◽  
Author(s):  
Sanjay Manohar ◽  
Valerie Bonnelle ◽  
Masud Husain
Keyword(s):  
Parkinson’S Disease ◽  
Traumatic Brain Injury ◽  
Parkinson's Disease ◽  
Brain Injury ◽  
Neurological Disorders ◽  
Brain Regions ◽  
Brain Lesions ◽  
Attention Deficits ◽  
Higher Cognitive Functions ◽  
Real Challenge

Attention deficits are a frequent and particularly disabling consequence of many neurological disorders, from patients with focal brain lesions through to individuals with traumatic brain injury or neurodegenerative conditions, such as Parkinson’s disease. They are often associated with apparent confusion, fatigue, irritability, and increased time and effort to perform even simple everyday tasks, and constitute a real challenge for rehabilitation. In many cases, attention deficits may be crucial factors underlying failures of memory and higher cognitive functions, contributing to difficulties in resuming previous activities and independent daily living. Here the authors first consider four aspects of attention—selective, sustained, executive, and divided—together with brain regions and networks considered to underpin normal attention and disorders of attention. The authors focus on focal brain lesions, traumatic brain injury and Parkinson’s disease as important examples illustrating the effects of different brain pathologies on attention function.

scholarly journals Potential Metabolomic Linkage in Blood between Parkinson’s Disease and Traumatic Brain Injury

Metabolites ◽  
2018 ◽  
Vol 8 (3) ◽  
pp. 50 ◽  
Author(s):  
Massimo Fiandaca ◽  
Thomas Gross ◽  
Thomas Johnson ◽  
Michele Hu ◽  
Samuel Evetts ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Traumatic Brain Injury ◽  
Parkinson's Disease ◽  
Brain Injury ◽  
Glutamic Acid ◽  
High Performance ◽  
Specific Gene ◽  
Potential Association ◽  
Health And Disease ◽  
Mechanistic Basis

The etiologic basis for sporadic forms of neurodegenerative diseases has been elusive but likely represents the product of genetic predisposition and various environmental factors. Specific gene-environment interactions have become more salient owing, in part, to the elucidation of epigenetic mechanisms and their impact on health and disease. The linkage between traumatic brain injury (TBI) and Parkinson’s disease (PD) is one such association that currently lacks a mechanistic basis. Herein, we present preliminary blood-based metabolomic evidence in support of potential association between TBI and PD. Using untargeted and targeted high-performance liquid chromatography-mass spectrometry we identified metabolomic biomarker profiles in a cohort of symptomatic mild TBI (mTBI) subjects (n = 75) 3–12 months following injury (subacute) and TBI controls (n = 20), and a PD cohort with known PD (n = 20) or PD dementia (PDD) (n = 20) and PD controls (n = 20). Surprisingly, blood glutamic acid levels in both the subacute mTBI (increased) and PD/PDD (decreased) groups were notably altered from control levels. The observed changes in blood glutamic acid levels in mTBI and PD/PDD are discussed in relation to other metabolite profiling studies. Should our preliminary results be replicated in comparable metabolomic investigations of TBI and PD cohorts, they may contribute to an “excitotoxic” linkage between TBI and PD/PDD.

scholarly journals Distinct dopaminergic abnormalities in traumatic brain injury and Parkinson’s disease

2020 ◽  
Vol 91 (6) ◽  
pp. 631-637
Author(s):  
Peter Owen Jenkins ◽  
Andreas-Antonios Roussakis ◽  
Sara De Simoni ◽  
Niall Bourke ◽  
Jessica Fleminger ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Traumatic Brain Injury ◽  
Parkinson's Disease ◽  
Brain Injury ◽  
Rating Scale ◽  
Single Photon ◽  
Photon Emission ◽  
Striatal Dopamine ◽  
Cross Sectional ◽  
Severe Tbi

ObjectiveTraumatic brain injury (TBI) and rapid eye movement sleep behavioural disorder (RBD) are risk factors for Parkinson’s disease (PD). Dopaminergic abnormalities are often seen after TBI, but patients usually lack parkinsonian features. We test whether TBI, PD and RBD have distinct striatal dopamine abnormalities using dopamine transporter (DaT) imaging.Methods123I-ioflupane single-photon emission CT scans were used in a cross-sectional study to measure DaT levels in moderate/severe TBI, healthy controls, patients with early PD and RBD. Caudate and putamen DaT, putamen to caudate ratios and left-right symmetry of DaT were compared.Results108 participants (43 TBI, 26 PD, 8 RBD, 31 controls) were assessed. Patients with early PD scored significantly higher on the Unified Parkinson’s Disease Rating Scale motor subscale than other groups. Patients with TBI and PD had reduced DaT levels in the caudate (12.2% and 18.7%, respectively) and putamen (9.0% and 42.6%, respectively) compared with controls. Patients with RBD had reduced DaT levels in the putamen (12.8%) but not in the caudate compared with controls. Patients with PD and TBI showed distinct patterns of DaT reduction, with patients with PD showing a lower putamen to caudate ratio. DaT asymmetry was greater in the PD group than other groups.ConclusionsThe results show that patients with early PD and TBI have distinct patterns of striatal dopamine abnormalities. Patients with early PD and moderate/severe TBI showed similar reductions in caudate DaT binding, but patients with PD showed a greater reduction in putamen DaT and a lower putamen to caudate ratio. The results suggest that parkinsonian motor signs are absent in these patients with TBI because of relatively intact putaminal dopamine levels.

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