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.
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.
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.
Mild cognitive impairment (MCI) and early Alzheimer's disease (AD) present significant challenges in aging populations, as cognitive decline impacts daily life and overall well-being. There has been a growing interest in non-pharmacological interventions that can mitigate the progression of these conditions. This review explores the impact of various interventions, including physical activity, nutrition, cognitive training, and multidomain approaches, on cognitive function in individuals with MCI or early AD. Studies have demonstrated the potential of exercise, particularly aerobic and strength training, to improve cognitive health by preserving brain structure and function. Nutritional interventions, particularly those focusing on Mediterranean-style diets, offer promising cognitive benefits due to their anti-inflammatory properties. Cognitive training programs have shown improvements in specific cognitive domains, but results regarding their long-term effectiveness are still inconclusive. Multidomain interventions that combine exercise, nutrition, and cognitive training show potential for optimizing cognitive function and reducing the risk of further cognitive decline. However, while these studies offer promising results, more large-scale, long-term trials are needed to confirm the sustained impact of these interventions and identify the most effective strategies for preventing dementia.
Recent clinical trials on cancer immunotherapy drugs have demonstrated improved breast cancer patient outcomes. Pembrolizumab, a cancer immunotherapy checkpoint inhibitor, has been utilized in clinical breast cancer trials due to its reasonable safety profile. Pembrolizumab acts on cancer cells by blocking programmed death-ligand-1 (PD-L1), allowing our adaptive immune system to function as it normally would. PD-L1 is a cell surface protein that induces T cell apoptosis upon binding to PD-1 receptors on T cells, a key mechanism for immune evasion. Through measuring overall response rate (ORR) and pathological complete response (pCR), researchers have measured the efficacy of Pembrolizumab. While it was generally found that there was no statistically significant difference for ORR, the data collected for pCR shows a statistically significant difference in patients who received pembrolizumab treatment compared to those who received the control. This data offers promising results that pembrolizumab could potentially improve breast cancer patient survival outcomes.
Sex-chromosome mutations are among the most detrimental to human health. Most are lethal or result in major loss of function, and their germline location allows mutations to affect multiple generations. A mosaic mutation causes an individual to have multiple populations of cells with different genotypes [1]. There are two types of mosaic chromosomal mutations (mCAs) that occur in germline cells. One has links to the Y chromosome in men (mLOY) while the other has links to the X chromosome in women (mLOX) [2].
