Detection of misfolded protein aggregated in HIV‐infected people

Abstract

AbstractBackgroundMany 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.MethodIn 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).ResultWe 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.ConclusionThis 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.