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Obesity is a chronic disease marked by the buildup of extra adipose tissue and a higher chance of developing concomitant illnesses such as heart disease, diabetes, high blood pressure, and some malignancies. Over the past few decades, there has been a global increase in the prevalence of obesity, which now affects around one-third of the world's population. According to recent studies, a variety of factors, including genetics and biology as well as environmental, physiological, and psychosocial factors, may have a role in the development of obesity. The prevalence of obesity is often higher among Hispanic American groups than among White people in the U.S. Obesity is a widespread condition with a high risk of morbidity and death, and it is well-recognized that the prevalence of comorbidities rises with rising levels of obesity or body mass index. To combat the rising prevalence of obesity in the USA, especially among Hispanics, one of the fastest-growing racial/ethnic groups in the country, there is an urgent need for obesity therapies. The exact cause of this disparity is unclear, but some responsible factors are a lack of education, high unemployment rates, high levels of food insecurity, an unhealthy diet, inadequate access to physical activity resources, a lack of health insurance, and constricted access to culturally adequate healthcare. Additionally, managing obesity and giving needed/timely support to obese people is a difficult responsibility for medical professionals and their loved ones. The need for caregivers is increasing with the increased number of individuals with obesity, particularly Hispanics. Our article summarizes the status of obesity, focusing on Hispanic populations, and we also highlight specific factors that contribute to obesity, including genetics, epigenetics, biological, physiological, and psychosocial factors, medication and disease, environment, and socio-demographics. This article also reviews caregiver duties and challenges associated with caring for people with obesity.
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Alzheimer's disease (AD) is the most widespread form of neurodegenerative disorder that causes memory loss and multiple cognitive issues. The underlying mechanisms of AD include the build-up of amyloid-ß and phosphorylated tau, synaptic damage, elevated levels of microglia and astrocytes, abnormal microRNAs, mitochondrial dysfunction, hormonal imbalance, and age-related neuronal loss. However, the etiology of AD is complex and involves a multitude of environmental and genetic factors. Currently, available AD medications only alleviate symptoms and do not provide a permanent cure. Therefore, there is a need for therapies that can prevent or reverse cognitive decline, brain tissue loss, and neural instability. Stem cell therapy is a promising treatment for AD because stem cells possess the unique ability to differentiate into any type of cell and maintain their self-renewal. This article provides an overview of the pathophysiology of AD and existing pharmacological treatments. This review article focuses on the role of various types of stem cells in neuroregeneration, the potential challenges, and the future of stem cell-based therapies for AD, including nano delivery and gaps in stem cell technology.
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Enfermedad de Alzheimer , Humanos , Enfermedad de Alzheimer/genética , Péptidos beta-Amiloides/metabolismo , Células Madre/metabolismo , Encéfalo/metabolismoRESUMEN
Obesity is a growing health concern in today's society. Current estimates indicate that obesity occurs in both adults and young people. Recent research also found that the Hispanic population in the U.S. is 1.9 times more likely to be overweight as compared to their non-Hispanic population. Obesity is a multifactorial disease that has a variety of causes. All current treatment options incorporate dietary changes aimed at establishing a negative energy balance. According to current scientific research, multiple factors are involved with the development of obesity, including genetic, biochemical, psychological, environmental, behavioral, and socio-demographic factors. The people who suffer from obesity are far more likely to suffer serious health problems, such as stroke, diabetes, lung disease, bone and joint disease, cancer, heart disease, neurological disorders, and poor mental health. Studies indicate that multiple cellular changes are implicated in the progression of obesity, mitochondrial dysfunction, deregulated microRNAs, inflammatory changes, hormonal deregulation, and others. This article highlights the role that oxidative stress plays in obesity and current obesity-prevention techniques with an emphasis on the impact of catechins to prevent and treat obesity.
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Alzheimer's disease (AD) is characterized by the accumulation of amyloid ß and phosphorylated τ protein aggregates in the brain, which leads to the loss of neurons. Under the microscope, the function of mitochondria is uniquely primed to play a pivotal role in neuronal cell survival, energy metabolism, and cell death. Research studies indicate that mitochondrial dysfunction, excessive oxidative damage, and defective mitophagy in neurons are early indicators of AD. This review article summarizes the latest development of mitochondria in AD: 1) disease mechanism pathways, 2) the importance of mitochondria in neuronal functions, 3) metabolic pathways and functions, 4) the link between mitochondrial dysfunction and mitophagy mechanisms in AD, and 5) the development of potential mitochondrial-targeted therapeutics and interventions to treat patients with AD.
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With increasing aging, dementia is a growing public health concern globally. Patients with dementia have multiple psychological and behavioral changes, including depression, anxiety, inappropriate behavior, paranoia, agitation, and hallucinations. The major types of dementia are Alzheimer's disease (AD), vascular dementia (VCID), Lewy body dementia (LBD), frontotemporal dementia (FTD), and mixed dementia (MiAD). Among these, AD is the most common form of dementia in the elderly population. In the last three decades, tremendous progress has been made in understanding AD's biology and disease progression, particularly its molecular basis, biomarker development, and drug discovery. Multiple cellular changes have been implicated in the progression of AD, including amyloid beta, phosphorylated tau, synaptic damage, mitochondrial dysfunction, deregulated microRNAs, inflammatory changes, hormonal deregulation, and others; based on these changes, therapeutic strategies have been developed, which are currently being tested in animal models and human clinical trials. The purpose of our article is to highlight recent therapeutic strategies' developments, critically discuss current strategies' failures, and propose new strategies to combat this devasting mental illness.
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Alzheimer's disease (AD) is the leading cause of dementia in elderly people. Amyloid beta (Aß) deposits and neurofibrillary tangles are the major pathological features in an Alzheimer's brain. These proteins are highly expressed in nerve cells and found in most tissues. Tau primarily provides stabilization to microtubules in the part of axons and dendrites. However, tau in a pathological state becomes hyperphosphorylated, causing tau dysfunction and leading to synaptic impairment and degeneration of neurons. This article presents a summary of the role of tau, phosphorylated tau (p-tau) in AD, and other tauopathies. Tauopathies, including Pick's disease, frontotemporal dementia, corticobasal degeneration, Alzheimer's disease, argyrophilic grain disease, progressive supranuclear palsy, and Huntington's disease, are the result of misprocessing and accumulation of tau within the neuronal and glial cells. This article also focuses on current research on the post-translational modifications and genetics of tau, tau pathology, the role of tau in tauopathies and the development of new drugs targeting p-tau, and the therapeutics for treating and possibly preventing tauopathies.
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Enfermedad de Alzheimer , Enfermedad de Pick , Tauopatías , Humanos , Anciano , Enfermedad de Alzheimer/metabolismo , Péptidos beta-Amiloides , Tauopatías/metabolismo , Proteínas tau/metabolismo , Enfermedad de Pick/metabolismo , Ovillos Neurofibrilares/metabolismoRESUMEN
Chronic conditions such as obesity, diabetes, and dementia are increasing in the United States (US) population. Knowledge of these chronic conditions, preventative measures, and proper management tactics is important and critical to preventing disease. The overlap between obesity, diabetes, and dementia is becoming further elucidated. These conditions share a similar origin through the components of increasing age, gender, genetic and epigenetic predispositions, depression, and a high-fat Western diet (WD) that all contribute to the inflammatory state associated with the development of obesity, diabetes, and dementia. This inflammatory state leads to the dysregulation of food intake and insulin resistance. Obesity is often the cornerstone that leads to the development of diabetes and, subsequently, in the case of type 2 diabetes mellitus (T2DM), progression to "type 3 diabetes mellitus (T3DM)". Obesity and depression are closely associated with diabetes. However, dementia can be avoided with lifestyle modifications, by switching to a plant-based diet (e.g., a Mediterranean diet (MD)), and increasing physical activity. Diet and exercise are not the only treatment options. There are several surgical and pharmacological interventions available for prevention. Current and future research within each of these fields is warranted and offers the chance for new treatment options and a better understanding of the pathogenesis of each condition.
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Demencia , Diabetes Mellitus Tipo 2 , Dieta Mediterránea , Resistencia a la Insulina , Demencia/etiología , Diabetes Mellitus Tipo 2/complicaciones , Diabetes Mellitus Tipo 2/epidemiología , Humanos , Obesidad/complicaciones , Obesidad/epidemiologíaRESUMEN
DiGeorge syndrome, caused by a microdeletion of the 22q11.2 region of chromosome 22, is a relatively rare condition. This syndrome can be difficult to recognize because a constellation of symptoms show different presentations. Most individuals diagnosed with this condition are identified in early childhood. With the emergence of new screening techniques, even fewer individuals with this syndrome are missed. Prior to these screening techniques, it was uncommon for patients to be diagnosed in adulthood. As a result, many internists, who focus only on the adult population, are unlikely to recognize and diagnose DiGeorge syndrome as the patient ages merely because it is not commonly diagnosed later in life. Early recognition and management are essential for the treatment of this condition. Here, we present the case of a 21-year-old woman diagnosed with DiGeorge syndrome as an adult.