Depressive disorder and neurodegenerative diseases are two different clinical entities. Depression is a common psychiatric disorder in the general population. However, when present concomitantly with neurodegenerative disorders, its diagnosis becomes challenging. In many cases, patients remain undiagnosed and hence, untreated, worsening the prognosis of the neurodegenerative diseases and impairing the quality of life. One of the possible reasons for the difficulties in diagnosis in such cases is that both conditions affect the central nervous system, so there might be an overlap of symptoms leading to a missed diagnosis of depression in a neurodegenerative disease patient and vice versa. Symptoms such as irritability, apathy, and decreased cognition are common to both types of disorders. Some neurodegenerative diseases, especially Alzheimer's disease, can initially present as a depressive prodrome. This may cause a difficulty in differentiating between these two conditions and a diagnosis of either conditions may be missed; hence an opportunity for timely intervention and improved outcomes is missed. An approach towards analyzing and comparing the pathological mechanisms common to both disease types will create a better understanding of depression and neurodegenerative diseases, identify their similarities, and develop improved clinical criteria to help clinicians make a timely diagnosis of these conditions present together. In the present review, various studies related to common pathological links, concomitant diagnosis challenges, and ongoing research about different treatment options are discussed.
Hemoglobin A1c (HbA1c) is a popular invaluable tool in the diagnosis of Type 2 diabetes for red blood cells (RBCs) with a lifespan of 120 days; however, many factors, including hemoglobinopathies, affect its accuracy. Sickle cell trait, primarily a benign medical condition, is a point mutation in only one of two beta-globin genes on chromosome 11. We performed a traditional review to identify how the sickle cell trait (SCT) affects the interpretation of HbA1c and the further implications it may have on the diagnosis and management of Type 2 diabetes. A literature search was performed using PubMed®/MEDLINE® and Google Scholar with formulated keywords (sickle cell trait, HbAS, HbA1c, glycosylated hemoglobin, diabetes, RBC lifespan, race, and genetics), with the majority of results being mainly observational studies. The National Glycohemoglobin Standardization Program (NGSP) is responsible for standardizing HbA1c results and also highlights factors that can interfere with HbA1c, including hemoglobin variants. Studies that utilize only an NGSP-certified method with no clinically significant interference by HbS in patients with and without SCT showed contrasting results. Additional studies showed that persons of African ancestry, the group to which the majority of SCT patients belong, have a higher HbA1c than non-Hispanic whites (NHWs), just based on race, and a greater probability of having glucose-6-phosphate dehydrogenase (G6PD) deficiency, which lowers HbA1c. The most extensive study investigating the RBC lifespan in SCT patients showed a reduction in the cell lifespan compared to normal patients; however, other smaller studies were contradictory. Our study highlights the need for hemoglobinopathy detection before or during HbA1c measurement in populations with a high degree of African ancestry and the importance of patient notification. It also shows that SCT affects the accuracy of HbA1c, through its likely reduction of RBC lifespan and its increased association with African ancestry and G6PD deficiency. This review recommends that for SCT patients with potential Type 2 diabetes, HbA1c should be used in combination with another diagnostic tool such as fasting blood glucose, fructosamine, or glycated albumin to decrease the chances of a missed diagnosis.
Multiple sclerosis (MS) is a neurodegenerative disease with a complex autoimmune component, and it has a high prevalence among middle-aged females. The manifestations of the disease range from episodic somatosensory dysfunction to progressive and permanent central nervous system (CNS) damage. Due to a high prevalence of psychiatric comorbidities and proven abnormalities in serotonin (5-HT) levels among MS patients, they are usually on drugs that modify the serotonergic system. Through a comprehensive literature review of studies published in the last 10 years related to 5-HT in MS and its therapeutic applications, we aimed to elucidate the mechanism behind the neurotransmitter (NT) levels' abnormalities. Most importantly, we endeavored to gather the most up-to-date information about the full therapeutic potential of agents acting on this system. We discovered that multiple processes cause low levels of 5-HT in MS patients. The varying levels of the availability of the 5-HT transporter (SERT) in the CNS decreasing overall tryptophan (TRP) levels, and diversion of the amino acid away from its synthetic pathway constitute some of those. Studies in animals have shown that 5-HT levels' elevations could cause immune-modulating effects and could probably slow down the disease progression rate. Human studies have shown a more diverse and complex response. Promising results have been obtained in the last 10 years regarding 5-HT's immunemodulatory role in MS patients and its therapeutic applications. Human studies with a larger population and feasible designs are still needed to fully ascertain the effects of serotonin on the immune system and disease progression in patients with MS.
The prevalence of dementia is around 5% worldwide in people above 65 years, which increases with aging. Alzheimer's disease is the most common cause of dementia in the elderly. On the other hand, anemia is considered one of the most prevalent comorbidities in the elderly with a prevalence of 11% in those above the age of 65. It is crucial that we find the association between anemia and dementia, as this linkage can prove beneficial. Many currently conducted studies support the idea that anemia is a significant risk factor for dementia. However, some studies still consider anemia and dementia as just an aging process, nothing more. In our study, we found that there are a lot of theories, such as low brain hemoglobin associated with low oxygen levels, which leads to neuron damage. One article mentioned that it is dependent on the level of hemoglobin as an effect with mild to moderate anemia, but apparent with severe forms of it. Researchers are expected to further explore and identify the exact relationship between anemia and dementia. We used the PubMed database as the principal source for data search and extracted articles exploring the relationship and role of anemia in decreasing the cognitive brain functions in the elderly. We reviewed 35 different articles, including clinical trials, review papers, randomized controlled trials (RCTs), and original research published between 2010 and 2020 to find commonly accepted pathophysiology that highlights how anemia causes a decrease in cognitive brain functions.
Paroxysmal supraventricular tachycardia (PSVT) is a common tachyarrhythmia, and an electrocardiogram is the best tool for making a diagnosis. If Valsalva maneuvers and carotid sinus massage do not give positive results, then the next choice is either adenosine or calcium channel blockers. At this time, adenosine is the drug of choice of treatment. Verapamil and diltiazem are the most commonly used calcium channel blockers (CCBs). This review aimed to compare the efficacy of both drugs in the treatment of PSVT.We utilized the databases PubMed Central and Medline by using keywords: "calcium channel blockers OR adenosine AND supraventricular tachycardia." In the end, we finalized 32 studies, including observational studies, literature reviews, systematic reviews/metanalysis, and randomized control trials. We included articles only in the English language and related to humans. Two authors completed the quality assessment and evaluation of bias according to specific guidelines. Only high-quality studies were included in this systematic review based on the cut-off score of seven or above. Calcium channel blockers have a longer halflife than adenosine and were previously used as the drug of choice in the treatment of PSVT. Calcium channel blockers are safe if given slowly; however, adenosine is safer and useful when an electrocardiogram is uncertain. We compared both drugs in certain aspects and found equal efficacy. Though safer, adenosine was found to have a higher cost and a higher probability of re-initiation arrhythmia compared to calcium channel blockers.
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