Systemic Infections May Cause Cognitive Deterioration and Neurodegeneration*

Chiu, Ming‐Jang

doi:10.1097/ccm.0000000000000205

Cited by 6 publications

(5 citation statements)

References 15 publications

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“…The potential mechanisms are multiple. Prolonged immobility during hospitalization accentuates muscle-atrophy and levels of proinflammatory cytokines, which further lead to muscle loss and sarcopenia (38,39). Decreased caloric and nutritional intake is a common feature of infectious diseases; this can negatively affect muscle health and function.…”

Section: Post-covid-19 Implicationsmentioning

confidence: 99%

“…About the impact of infections on cognitive function, many studies supported the possibility that pneumonia, and virus infection to a lesser extent, negatively affect cognition. The neurotrophic propensity of the virus and the sustained pro-inflammatory status induced by the infection may trigger or accelerate neurodegenerative processes through increased deposition of beta-amyloid and microglia activation ( 35 , 40 – 42 ). Similarly, the systemic inflammatory status and the boost in the oxidative processes might explain the impact of pneumonia on cognition.…”

Section: Post-covid-19 Implicationsmentioning

confidence: 99%

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Frailty Pathogenesis, Assessment, and Management in Older Adults With COVID-19

She

Chen

et al. 2021

Front. Med.

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The 2019 coronavirus disease (COVID-19) is a highly contagious and deadly disease. The elderly people are often accompanied by chronic inflammation and immunodeficiency, showing a frail state. The strength, endurance, and physiological function of the elderly are significantly decreased, and the ability to deal with stress response is weakened. They are the high-risk group that suffering from COVID-19, and rapidly developing to critical illness. Several recent studies suggest that the incidence rate of COVID-19 in elderly patients with frailty is high. Early assessment, detection, and effective intervention of frailty in COVID-19 patients are conducive to significantly improve the quality of life and improve prognosis. However, there are insufficient understanding and standards for the current evaluation methods, pathogenesis and intervention measures for COVID-19 combined with frailty. This study reviews the progress of the research on the potential pathogenesis, evaluation methods and intervention measures of the elderly COVID-19 patients with frailty, which provides a reference for scientific and reasonable comprehensive diagnosis and treatment in clinical.

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Section: Post-covid-19 Implicationsmentioning

confidence: 99%

Section: Post-covid-19 Implicationsmentioning

confidence: 99%

Frailty Pathogenesis, Assessment, and Management in Older Adults With COVID-19

She

Chen

et al. 2021

Front. Med.

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“…The neurotrophic properties of the virus and the infection-induced sustained pro-inflammatory state facilitate neurodegenerative processes through increased beta-amyloid deposition and microglia activation [ 48 , 49 , 50 , 51 ], leading to Alzheimer’s and Parkinson’s disease, which are the two most common pathological manifestations. Indeed, a systemic inflammatory status and increased oxidative processes could explain the impact of pneumonia on cognition.…”

Section: Physiological Aging: From Frailty To Susceptibility To Neuro...mentioning

confidence: 99%

Parkinson’s Disease, SARS-CoV-2, and Frailty: Is There a Vicious Cycle Related to Hypovitaminosis D?

et al. 2023

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The literature has long established the association between aging and frailty, with emerging evidence pointing to a relationship between frailty and SARS-CoV-2 contagion. The possible neurological consequences of SARS-CoV-2 infection, associated with physical and cognitive frailty, could lead to a worsening of Parkinson’s disease (PD) in infected patients or—more rarely—to an increase in the Parkinsonian symptomatology. A possible link between those clinical pictures could be identified in vitamin D deficiency, while the whole process would appear to be associated with alterations in the microbiota–intestine–brain axis that fall within the α-Synuclein Origin site and Connectome (SOC) model, and allow for the identification of a body-first PD and a brain-first PD. The model of care for this condition must consider intrinsic and extrinsic variables so that care by a multidisciplinary team can be successfully predicted. A multidimensional screening protocol specifically designed to identify people at risk or in the early stages of the disease should begin with the investigation of indices of frailty and microbiota–intestine–brain axis alterations, with a new focus on cases of hypovitaminosis D.

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“…Several potential mechanisms have been hypothesized to explain the association of pneumonia and varicella zoster with cognitive aging. The neurotrophic propensity of the virus and the sustained pro-inflammatory status induced by the infection may trigger or accelerate neurodegenerative processes through increased deposition of beta-amyloid and microglia activation ( Chiu, 2014 ; Hokkanen et al, 1997 ; Iwashyna et al, 2010 ; Reichenberg et al, 2001 ). Similarly, the systemic inflammatory status and the boost in the oxidative processes might explain the impact of pneumonia on cognition.…”

Section: Infections and Frailtymentioning

confidence: 99%