Viral mimetic priming enhances α-synuclein-induced degeneration: Implications for Parkinson’s disease

Olsen, Laura; Cairns, Andrew G.; Ådén, Jörgen; Moriarty, Niamh; Cabré, Sílvia; Alamilla, Verónica; Almqvist, Fredrik; Dowd, Eilís; McKernan, Declan P.

doi:10.1016/j.bbi.2019.04.036

Cited by 22 publications

(26 citation statements)

References 70 publications

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“…26 Information as to permanency is of considerable significance, because loss of the ability to smell significantly impacts quality of life, the flavor of foods, and beverages, and safety from spoiled food, fire, and leaking natural gas. Importantly, smell loss can be a harbinger of a number of neurological diseases, most notably AD and PD—diseases which, in some cases, have been associated with a number of viruses 46,47 . Although the reasons are poorly understood, older persons with smell loss are 3 times more likely to die over the course of an ensuring half‐decade than older persons with a normal sense of smell 48,49 …”

Section: Discussionmentioning

confidence: 99%

Smell dysfunction: a biomarker for COVID‐19

Moein

Hashemian

Mansourafshar

et al. 2020

Int Forum Allergy Rhinol

739

859

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Background: Severe acute respiratory syndromecoronavirus-2 (SARS-CoV-2), the virus that causes coronavirus disease 2019 (COVID-19), is responsible for the largest pandemic since the 1918 influenza A virus subtype H1N1 influenza outbreak. The symptoms presently recognized by the World Health Organization are cough, fever, tiredness, and difficulty breathing. Patient-reported smell and taste loss has been associated with COVID-19 infection, yet no empirical olfactory testing on a cohort of COVID-19 patients has been performed. Methods: The University of Pennsylvania Smell Identification Test (UPSIT), a well-validated 40-odorant test, was administered to 60 confirmed COVID-19 inpatients and 60 age-and sex-matched controls to assess the magnitude and frequency of their olfactory dysfunction. A mixed effects analysis of variance determined whether meaningful differences in test scores existed between the 2 groups and if the test scores were differentially influenced by sex. Results: Fi y-nine (98%) of the 60 patients exhibited some smell dysfunction (mean [95% CI] UPSIT score: 20.98 [19.47, 22.48]; controls: 34.10 [33.31, 34.88]; p < 0.0001). Thirty-five of the 60 patients (58%) were either anosmic (15/60; 25%) or severely microsmic (20/60; 33%); 16 exhibited moderate microsmia (16/60; 27%), 8 mild microsmia (8/60; 13%), and 1 normosmia (1/60; 2%). Deficits were evident for all 40 UPSIT odorants. No meaningful relationships between the test scores and sex, disease severity, or comorbidities were found. Conclusion: Quantitative smell testing demonstrates that decreased smell function, but not always anosmia, is a major marker for SARS-CoV-2 infection and suggests the possibility that smell testing may help, in some cases, to identify COVID-19 patients in need of early treatment or quarantine.

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Section: Discussionmentioning

confidence: 99%

Smell dysfunction: a biomarker for COVID‐19

Moein

Hashemian

Mansourafshar

et al. 2020

Int Forum Allergy Rhinol

739

859

View full text Add to dashboard Cite

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“…We know from both inflammatory animal models of PD and from clinical studies that neuroinflammation is an important component of disease progression in PD [40][41][42]. It has also been documented that there is an increase in peripheral inflammation in PD patients.…”

Section: Viral Infection and Pdmentioning

confidence: 99%

Back to the future: lessons from past viral infections and the link with Parkinson’s disease

Dowd

McKernan

2021

Neuronal Signaling

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During the current COVID-19 pandemic, there has been noticeable increase in the reporting of neurological symptoms in patients. There is still uncertainty around the significance and long-term consequence of these symptoms. There are also many outstanding questions on whether the causative virus SARS-CoV2 can directly infect the central nervous system. Given the long association between viral infections with neurodegenerative conditions such as Parkinson’s disease, it seems timely to review this literature again in the context of the COVID-19 pandemic and to glean some useful information from studies on similar viruses. In this commentary, we will consider the current knowledge on viral infections in the brain. In addition, we review the link between viral infection and neurodegeneration in Parkinson’s disease, and review the recent literature on SARS infections, the potential link with Parkinson’s disease and the potential areas of study in the future

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“…In animal models of neurodegenerative disease, a systemic inflammatory challenge has been shown to produce an exaggerated immune response in the CNS [112,113]. Olsen et al [114] also demonstrated that viral neuroinflammatory priming in the substantia nigra significantly exacerbated α-synuclein aggregate-induced neuroinflammation and neurodegeneration. Another group likewise observed an enhanced neurodegenerative effect by combination of the H1N1 influenza virus and MPTP [115].…”

Section: Microglial Role In Chronic Neuroinflammation and Neurodegenementioning

confidence: 99%

Microglial Phenotypes and Their Relationship to the Cannabinoid System: Therapeutic Implications for Parkinson’s Disease

et al. 2020

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Parkinson’s disease is a neurodegenerative disorder, the motor symptoms of which are associated classically with Lewy body formation and nigrostriatal degeneration. Neuroinflammation has been implicated in the progression of this disease, by which microglia become chronically activated in response to α-synuclein pathology and dying neurons, thereby acquiring dishomeostatic phenotypes that are cytotoxic and can cause further neuronal death. Microglia have a functional endocannabinoid signaling system, expressing the cannabinoid receptors in addition to being capable of synthesizing and degrading endocannabinoids. Alterations in the cannabinoid system—particularly an upregulation in the immunomodulatory CB2 receptor—have been demonstrated to be related to the microglial activation state and hence the microglial phenotype. This paper will review studies that examine the relationship between the cannabinoid system and microglial activation, and how this association could be manipulated for therapeutic benefit in Parkinson’s disease.

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Viral mimetic priming enhances α-synuclein-induced degeneration: Implications for Parkinson’s disease

Cited by 22 publications

References 70 publications

Smell dysfunction: a biomarker for COVID‐19

Smell dysfunction: a biomarker for COVID‐19

Back to the future: lessons from past viral infections and the link with Parkinson’s disease

Microglial Phenotypes and Their Relationship to the Cannabinoid System: Therapeutic Implications for Parkinson’s Disease

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