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Neurodegenerative diseases, such as Alzheimer's disease (AD), are a growing public health crisis, exacerbated by an aging global population and the lack of effective early disease-modifying therapies. Early detection of neurodegenerative disorders is critical to delaying symptom onset and mitigating disease progression, but current diagnostic tools often rely on detecting pathology once clinical symptoms have emerged and significant neuronal damage has already occurred. While disease-specific biomarkers, such as amyloid-beta and tau in AD, offer precise insights, they are too limited in scope for broader neurodegeneration screening for these conditions. Conversely, general biomarkers like neurofilament light chain (NfL) provide valuable staging information but lack targeted insights. Circulating cell-free DNA (cfDNA), released during cell death, is emerging as a promising biomarker for early detection. Derived from dying cells, cfDNA can capture both general neurodegenerative signals and disease-specific insights, offering multi-layered genomic and epigenomic information. Though its clinical potential remains under investigation, advances in cfDNA detection sensitivity, standardized protocols, and reference ranges could establish cfDNA as a valuable tool for early screening. cfDNA methylation signatures, in particular, show great promise for identifying tissue-of-origin and disease-specific changes, offering a minimally invasive biomarker that could transform precision neurology. However, further research is required to address technological challenges and validate cfDNA's utility in clinical settings. Here, we review recent work assessing cfDNA as a potential early biomarker in AD. With continued advances, cfDNA could play a pivotal role in shifting care from reactive to proactive, improving diagnostic timelines and patient outcomes. [ABSTRACT FROM AUTHOR]

Neurocysticercosis is a leading cause of seizures and epilepsy in the developing world. Cysticercosis is endemic in many regions of Central and South America, sub-Saharan Africa, India, and Asia. Neurocysticercosis is of emerging importance because globalization has increased travel between Hawai'i and disease-endemic areas. Headache and epilepsy are two of the most common complications of neurocysticercosis infection. Currently, it is not known if epilepsy patients with neurocysticercosis are more likely to have headaches than those with other structural brain lesions or those with no structural brain abnormalities. This study was designed to investigate whether epilepsy patients with neurocysticercosis report co-morbid headaches more frequently than those with other or with no structural brain lesions. A retrospective cross-sectional study of all patients treated at a community based neurology clinic for epilepsy during a three-month period was performed. One-hundred sixty patients were included in the analytical study. Co-morbid headaches were more commonly present among those with neurocysticercosis (40%) than those with other structural lesions and those with no structural brain abnormalities (19% and 22%, respectively; P = .031). Headache frequency among those reporting co-morbid headaches did not differ significantly between the groups. Prevalence of co-morbid headaches is greater among epilepsy patients with neurocysticercosis than those with other structural brain lesions or no structural brain abnormality. Epilepsy patients with neurocysticercosis may be especially vulnerable to development of headaches and a thorough headache history should be obtained to help screen for affected individuals. [ABSTRACT FROM AUTHOR]

Introduction: Calcified parenchymal neurocysticercosis (NCC) lesions are commonly detected in many individuals with refractory epilepsy. However, the relationship between these lesions and epilepsy is not fully determined. We sought to determine if calcified parenchymal NCC demonstrated topographic congruence with epileptiform activity in refractory epilepsy patients. Additional patients with other structural brain lesions were included for comparison. Subjects and Methods: Retrospective cross-sectional analysis of all patients treated at a community-based neurology clinic for refractory epilepsy during a 3-month period and with structural brain lesions detected by neuroimaging studies. Results: A total of 105 patients were included in the study, including 63 with calcified parenchymal NCC lesions and 42 with other structural brain lesions. No significant relationship was detected between hemispheric localization of calcified parenchymal NCC lesions and epileptiform activity. For those with other structural brain lesions, the hemispheric localization was significantly related to the side of epileptiform activity (Chi-square = 11.13, P = 0.025). In addition, logistic regression models showed that those with right-sided non-NCC lesions were more likely to have right-sided epileptiform activity (odds ratio = 4.36, 95% confidence interval [CI] =1.16-16.31, P = 0.029), and those with left-sided non-NCC lesions were more likely to have left-sided epileptiform activity (odds ratio = 7.60, 95% CI = 1.89-30.49, P = 0.004). Conclusion: The lack of correlation between the side of calcified parenchymal NCC lesions and the side of the epileptiform activity suggests that these lesions may be incidental findings in many patients. [ABSTRACT FROM AUTHOR]

In bilingual individuals, regression to a primary language may be associated with development of cognitive impairment and increased risk for development of dementia. This report describes two bilingual patients who presented with early symptoms of dementia after regression to their primary language. The results of this study may help clinicians identify aging bilingual patients who are beginning to develop cognitive impairment or dementia and suggest that further studies on the long term cognitive effects of bilingualism and interactions with the aging process are indicated. [ABSTRACT FROM AUTHOR]

The article offers an overview of the Center for Native and Pacific Health Disparities Research and its components designed to reduce and eliminate cardiometabolic disparities in Native Hawaiians, Alaska Natives and other Pacific Island Peoples in the U.S. It states that the Center adopts research known as Community-Based Participatory Research (CBPR) to guide community-academic partnerships. The Center is comprised of interdisciplinary researchers and scientists in order to address the need for developing innovative interventions in managing diseases.

Background: The relationship between cigarette smoking and development of Alzheimer's disease (AD) is not fully determined, and previous reports disagree, with some studies suggesting an increased relative risk and others a decreased odds ratio. Consequently, we wanted to determine if the prevalence of past cigarette smoking observed in a community-based clinic sample of patients with AD would be more consistent with the expected value obtained from a model using either an increased relative risk or a decreased odds ratio to estimate the effect of smoking on development of AD., Materials and Methods: Retrospective cross-sectional analysis of all patients treated for AD in a community-based Neurology Clinic during a 2-year period. Estimates of expected past smoking prevalence were calculated based on published values for either an increased relative risk or a decreased odds ratio and compared to the past smoking prevalence observed in the clinic sample., Results: The observed past smoking prevalence in the clinic population was 29.17%. The expected past smoking prevalence calculated using the increased relative risk was 30.07% (95% confidence interval [CI] = 27.67-32.32%), and using the decreased odds ratio was 12.54% (95% CI = 6.32-24.81%)., Conclusion: The observed past smoking prevalence among the patients being treated for AD in a community-based clinic falls within the expected 95% CI for the increased relative risk model and outside of the expected 95% CI for the decreased odds ratio model. These results support the contention that the relationship between cigarette smoking and development of AD is the best characterized by an increased relative risk., Competing Interests: There are no conflicts of interest.

Parkinson's disease is associated with progressive degeneration of mesolimbic dopaminergic neurons that are involved in reward-based behavior learning, including rewarding effects of food consumption and drugs of abuse. The importance of this pathway in development of addictive behaviors led us to hypothesize that medical disorders related to poor impulse control may occur less frequently among patients with Parkinson's disease than those with other progressive neurodegenerative disorders such as Alzheimer's disease. Retrospective cross-sectional study of all patients treated for Parkinson's disease and Alzheimer's disease in a community based clinic during a two-year period. Associations were summarized using odds ratios (OR) and 95% confidence intervals (95% CI) estimated from logistic regression models, adjusted for differences in gender distribution between the groups. A total of 106 patients with Parkinson's disease and 72 patients with Alzheimer's disease were included. Patients with Parkinson's disease were less likely to have either past substance use (adjusted OR = 0.035, 95% CI = 0.009 - 0.130) or presence of co-morbid medical conditions related to poor dietary choices (adjusted OR = 0.157, 95% CI = 0.062 - 0.397). Co-morbid medical conditions related to poor impulse control occur less frequently among those with Parkinson's disease than those with Alzheimer's disease. These findings are consistent with dysfunction of dopamine dependent pathways involved in addiction during the presymptomatic phase of Parkinson's disease and support a biological basis for addiction.

Objective: To compare the fast food outlets and exercise resources across 3 communities with varying percentages of Native Hawaiians (NH) and to correlate these findings with obesity prevalence., Methods: Data on all food and exercise resources were collected from January through July 2006 within a 1-mile radius in 3 distinct communities (site A = higher % NH to site C = lower % NH). Comparisons between communities were analyzed in 2007 using Fisher's Exact and ANOVA., Results: Trends in obesity prevalence paralleled the percentage of NHs. After adjusting for population size, site B had a greater number of fast food outlets (p < 0.001) than site A or C, and more exercise facilities compared to site A (p = 0.05). Availability of fast food outlets was significantly greater at site A compared to site C (p = 0.03). Usage of exercise facilities was not significantly different between sites although exercise resources were in 'poorer' condition at site A compared to site B or C (p < or = 0.05)., Discussion: Results confirm the increased frequency of obesogenic environmental factors and their correlation with obesity trends across 3 distinct NH communities. These results suggest that environmental factors may offer another means for reducing obesity disparities in minority communities.