According to Woolf and associates, U.S life expectancy increased from 69.9 years to 78.9 years between 1959 and 2016 [1]. With increasing age comes an array of medical morbidities, including cardiovascular disease, malignancy (cancer), and what some would argue as the most debilitating, cognitive decline [2].
Fetal Alcohol Syndrome Disorder (FASD) is characterized by a set of behaviors that are brought on by fetal alcohol exposure during utero, causing an abnormal neurodevelopmental process [3]. Despite it being preventable, approximately 2% to 5% of United States schoolchildren are impacted by prenatal alcohol exposure (PAE), with 6-9 out of 1,000 actually being diagnosed with this disorder [1,2,3]. Severe consequences of fetal ethanol exposure consist of miscarriages, stillbirths, and premature delivery [2].
Complex regional pain syndrome (CRPS), a neuroinflammatory disease, ranks number one on the McGill Pain Scale, topping fibromyalgia, cancer, and amputation without anesthetics. The development of CRPS typically occurs after trauma to the arm or leg (e.g., breaking of a bone, dislocation of a joint, surgical trauma to a limb) that results in a disproportionately high sensation of pain. This painful response is chronic and characterized by constant pain with additional flare-ups that last different amounts of time from person to person.
In the summer of 1940, soaring above the clouds 17,000 feet above Britain, the Allies and enemy German fighter planes filled the sky. Bright flashes of light illuminate the horizon, and smoke rises all around. Inside the cockpit, the cacophony of bullets raining around the plane and the rattling of the metal panels resonate. From the dogfight of the other planes, a stray bullet whizzes past.
Alzheimer’s disease is a progressive neurodegenerative disorder that affects an estimated 6.9 million Americans today, a figure expected to rise significantly with population aging [1]. As the most common cause of dementia, Alzheimer’s is a leading contributor to disability and dependency among older adults, placing an immense burden, both mental and fiscal, on patients, families, and healthcare systems. In 2023, over 11 million informal and unpaid caregivers in the U.S. provided 18.4 billion hours of care, valued at $346.6 billion [1].
Age-related neurodegenerative disease pathogenesis remains a hot topic for scientists as there are many ways to approach it: genome instability, protein misfolding, and neuronal defects, to name a few. There is, however, a consensus that dysfunctional autophagy is ubiquitous in neurodegenerative disease. Autophagy, the degradation of intracellular material, maintains homeostasis amidst cellular stress, yet its efficiency is lowered in diseases like Alzheimer’s and Parkinson’s. As cell stress accumulates over natural aging, how autophagy fails under cell stress overload is a key question for researchers. In neurodegenerative disease, there are multiple cell stressors present, three of which we will address: nutrient stress, endoplasmic reticulum (ER) stress, and mitochondrial stress. This review will examine three major autophagy pathways that respond to these stressors respectively—lipophagy, ER-phagy, and mitophagy—and their relationship with one another. Research typically focuses on individual autophagy mechanisms, but there is a lack of research on how these autophagy pathways relate to one another. We identify the nuclear-ER-vacuole junction as an intersection between lipophagy and ER-phagy, but it is harder to connect mitophagy with the two. While mitophagy also requires core autophagy machinery, it specifically relies on the cortical-ER instead of the nuclear-ER. How these connections are affected by neurodegenerative disease is less explored. As there are many different cell stressors present in neurodegenerative disease, the lack of a unifying approach to explain its pathogenesis emphasizes a need for future research that addresses the effects of simultaneous cell stress pathways on autophagy.
Nursing students spend years developing clinical skills, critical thinking, and the ability to provide safe, personalized care. Upon entering the workforce, however, they are thrown into wildly understaffed environments where they are expected to handle an excessive number of patients on their first day. While observing during internships, it became clear to me how burdened they are.
Malignant brain tumors are responsible for the deaths of many pediatric, adolescent, and adult populations around the world. It is estimated that 87,053 deaths were attributed to malignant brain tumors between 2017 and 2021, with brain cancer being the most common cause of cancer death amongst pediatric populations [1].
The exact mechanisms behind COVID-19-induced anosmia, or the complete loss of smell, remain unclear due to conflicting findings that fail to establish a direct and consistent link between viral presence, cellular damage, and the subsequent disruption of olfactory function and inflammation within the olfactory system. Anosmia affects nearly 19% of COVID-19 patients, lasting an average of two months after recovery, significantly reducing their quality of life [1].
Emerging evidence suggests that COVID is associated with a wide range of cardiac abnormalities in patients aged 30–50 years, including individuals with no prior cardiovascular risk factors. This review synthesizes five contemporary studies to evaluate the nature, persistence, and clinical implications of post-COVID cardiac dysfunction. Diagnostic approaches used in these studies included cardiac magnetic resonance imaging (CMR), echocardiography, and exercise testing. The use of these testing methodologies revealed subclinical impairments, structural remodeling, and diminished functional capacity. Additionally, persistent inflammation and abnormal global longitudinal strain were also frequently observed, often in the absence of other symptoms or elevated biomarkers. Despite variations in methodology and sample demographics, the studies converged on the conclusion that COVID poses a threat to cardiac health. Limitations of these studies included small cohort sizes, limited follow-up, and heterogeneity in diagnostic protocols, underscoring the need for standardized longitudinal research. The overall conclusion emphasizes the importance of proactive diagnostic screening and tailored treatment strategies to mitigate long-term cardiovascular consequences in this population.
