Publications by authors named "Lee Neilson"

Importance: The risk of developing Parkinson disease (PD) after objective hearing loss is unknown. PD studies using self-reported hearing loss are insensitive, and objective data are lacking.

Objective: To examine the association of hearing loss with incident PD in US veterans and its effect modification by well-established prodromal conditions and hearing aids.

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Introduction: The research criteria for prodromal Parkinson disease (pPD) depends on prospectively validated clinical inputs with large effect sizes and/or high prevalence. Neither traumatic brain injury (TBI), post-traumatic stress disorder (PTSD), nor chronic pain are currently included in the calculator, despite recent evidence of association with pPD. These conditions are widely prevalent, co-occurring, and already known to confer risk of REM behavior disorder (RBD) and PD.

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Huntington's disease (HD) is a devastating neurodegenerative disorder caused by aggregation of the mutant huntingtin (mHTT) protein, resulting from a CAG repeat expansion in the huntingtin gene HTT. HD is characterized by a variety of debilitating symptoms including involuntary movements, cognitive impairment, and psychiatric disturbances. Despite considerable efforts, effective disease-modifying treatments for HD remain elusive, necessitating exploration of novel therapeutic approaches, including lifestyle modifications that could delay symptom onset and disease progression.

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Article Synopsis
  • RBD is a sleep disorder that can lead to serious brain diseases like Parkinson's, especially in people with past brain injuries or stress.
  • People with both RBD and past trauma had their RBD symptoms start earlier and were more severe than those with just RBD.
  • The study found that those with both RBD and trauma experienced worse mental and physical health, suggesting a possible link to worsening brain problems over time.
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Background: Trauma-related disorders such as traumatic brain injury (TBI) and posttraumatic stress disorder (PTSD) are emerging as risk factors for Parkinson's disease (PD), but their association with development of PD and independence from comorbid disorders remains unknown.

Objective: To examine TBI and PTSD related to early trauma in military veterans using a case-control study.

Methods: PD was identified by International Classification of Diseases (ICD) code, recurrent PD-specific prescriptions, and availability of 5+ years of earlier records.

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As the prevalence of Parkinson's disease (PD) grows, so too does the population at-risk of developing PD, those in the so-called prodromal period. This period can span from those experiencing subtle motor deficits yet not meeting full diagnostic criteria or those with physiologic markers of disease alone. Several disease-modifying therapies have failed to show a neuroprotective effect.

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Objectives: To determine the relationship between the number of plasma exchanges and clinical outcome in patients experiencing myasthenic crisis.

Methods: We retrospectively reviewed all episodes of myasthenia gravis exacerbation/crisis who received plasmapheresis in patients admitted to a single-center tertiary care referral center from July 2008 to July 2017. We performed statistical analyses to determine whether the increased number of plasma exchanges improves the primary outcome (hospital length of stay) and the secondary outcome (disposition to home, skilled nursing facility, long-term acute care hospital, or death).

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Article Synopsis
  • Conventional MRI is useful for assessing multiple sclerosis (MS), but it has limitations in detecting early neurodegeneration and mainly shows late-stage brain atrophy.
  • There is a pressing need for biomarkers that can identify neurodegenerative processes before they become irreversible, particularly with the role of oxidative stress in MS pathogenesis being underexplored.
  • Recent advancements in imaging markers related to inflammation and neuronal integrity highlight the potential for non-invasive imaging to assess oxidative stress in real-time, which could enhance the understanding and management of MS and other neurodegenerative diseases.
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Background: Parkinson's disease is the second most common neurodegenerative disorder and presents with a heterogeneous group of symptoms. Managing these symptoms requires coordinated care from a neurology specialist and a primary care provider. Access to neurology care is limited for those patients with Parkinson's disease who reside in rural areas given financial and mobility constraints along with the rarity of specialty providers.

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Multiple System Atrophy (MSA) is a neurodegenerative disease with heterogeneous manifestations and is therefore difficult to diagnose definitively. Because of this, oftentimes an extensive workup for mimickers is undertaken. We herein report a case where the history and cerebrospinal fluid (CSF) findings of oligoclonal bands suggested an inflammatory disorder.

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Nuclear factor erythroid 2-related factor 2 (NRF2), a transcription factor which plays a critical role in maintenance of cellular redox, has been identified as a therapeutic target in a number of human diseases. Several reports have demonstrated beneficial effects of NRF2 manipulation in animal models of disease, and one NRF2-activating drug, dimethyl fumarate, is already approved for the treatment of multiple sclerosis. However, drug discovery is slowed due to a dearth of biomarkers which can inform target engagement and magnitude and duration of action.

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Background: Limb ischemia resulting from peripheral vascular disease is a common cause of morbidity. Vessel occlusion limits blood flow, creating a hypoxic environment that damages distal tissue, requiring therapeutic revascularization. Hypoxia-inducible factors (HIFs) are key transcriptional regulators of hypoxic vascular responses, including angiogenesis and arteriogenesis.

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Unlabelled: Neuroinflammation is an important contributor to Alzheimer's disease (AD) pathogenesis, as underscored by the recent identification of immune-related genetic risk factors for AD, including coding variants in the gene TREM2 (triggering receptor expressed on myeloid cells 2). Understanding TREM2 function promises to provide important insights into how neuroinflammation contributes to AD pathology. However, studies so far have produced seemingly conflicting results, with reports that amyloid pathology can be both decreased and increased in TREM2-deficient AD mouse models.

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Background: Alzheimer's disease (AD) is a multifactorial disorder associated with the accumulation of soluble forms of beta-amyloid (Aβ) and its subsequent deposition into plaques. One of the major contributors to neuronal death is chronic and uncontrolled inflammatory activation of microglial cells around the plaques and their secretion of neurotoxic molecules. A shift in microglial activation towards a phagocytic phenotype has been proposed to confer benefit in models of AD.

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