Since first described in the early 1900s, Alzheimer’s disease (AD) has risen exponentially in prevalence and concern. Research still drives to understand the etiology and pathogenesis of this disease and what risk factors can attribute to AD. With a majority of AD cases being of sporadic origin, the increasing exponential growth of an aged population and a lack of treatment, it is imperative to discover an easy accessible preventative method for AD. Some risk factors can increase the propensity of AD such as aging, sex, and genetics. Moreover, there are also modifiable risk factors—in terms of treatable medical conditions and lifestyle choices—that play a role in developing AD. These risk factors have their own biological mechanisms that may contribute to AD etiology and pathological consequences. In this review article, we will discuss modifiable risk factors and discuss the current literature of how each of these factors interplay into AD development and progression and if strategically analyzed and treated, could aid in protection against this neurodegenerative disease.

The causative agent of Chagas disease, Trypanosoma cruzi, is transmitted by triatomine vectors. The insect is endemic in the Americas, including the United States, where epidemiological studies are limited, particularly in the Southwestern region. Here, we have determined the prevalence of T. cruzi in triatomines, and feral cats and dogs, and wild animals, the infecting parasite genotypes and the mammalian host bloodmeal sources of the triatomines at four different geographical sites in the U.S.-Mexico border, including El Paso County, Texas, and nearby cities in New Mexico. Using qualitative polymerase chain reaction to detect T. cruzi infections, we found 66.4% (n = 225) of triatomines, 45.3% (n = 95) of feral dogs, 39.2% (n = 24) of feral cats, and 71.4% (n = 7) of wild animals positive for T. cruzi. Over 95% of T. cruzi genotypes or discrete typing units (DTUs) identified were TcI and some TcIV. Furthermore, Triatoma rubida was the triatomine species most frequently (98.2%) collected in all samples analyzed. These findings suggest a high prevalence of T. cruzi infections among triatomines, and feral and wild animals in the studied sites. Therefore, our results underscore the urgent need for implementation of a systematic epidemiological surveillance program for T. cruzi infections in insect vectors, and feral and wild animals, and Chagas disease in the human population in the southwestern region of the United States.

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Background Many people living with HIV (PLWH) develop dementia and cognitive dysfunction often referred as HIV‐associated neurocognitive disorder (HAND). The prevalence of HAND increases with age and considering that the number of PLWH aged 55 and older is increasing in the United States, it is expected that this number will also increase in the near future. The cellular and molecular mechanisms responsible for HAND are not well defined but evidence suggests many commonalities with Alzheimer’s disease and related neurodegenerative disorders. Method In the present study, we analyzed by histological analysis the presence of misfolded protein aggregates of amyloid‐β (Aβ) and Tau in the brain of 22 PLWH (67.41±1.48 y/o) and 15 controls (HIV negative, 73.87±2.93 y/o). Result We found a higher prevalence of Tau deposits in the brain of PLWH (N=9/22; 41%) in comparison with HIV‐negative controls (N=3/15; 20%). However, the co‐occurrence of Aβ and Tau pathology was more prevalent in controls (N=8/15; 53%) than in PLWH (N=7/22; 32%) samples. Conclusion This result may be due to the fact that the control group was significant older than the HIV‐infected group. More analyses with age‐matched groups are needed to clarify this finding. Our preliminary results suggest some differentiation between the groups with a higher prevalence of Aβ‐independent Tau pathology in HIV.