Background: We planned to analyze the prevalence and distribution of beta-amyloid deposition in the HIV+ brain in the HAART era. Our working hypothesis is that long term survival, aging and the secondary effects of HAART may contribute to increased beta-amyloid accumulation in this patient population.
Methods: Paraffin embedded archival brain autopsy tissues were assessed by immunocytochemistry for beta-amyloid. Detailed in-vivo neuro-behavioral assessments and ApoE genotyping were available for a subset of the studied population.
Results: Immunoreactivity with the antibodies 4G8 and 6E10 was found predominantly in neuronal soma and dystrophic axonal processes. Extracellular, often perivascular plaques were also identified in many cases.
Conclusions: We propose that prolonged HAART and aging may contribute to an overall increase in amyloid deposition, potentially mediated by inhibition of insulin degradation enzyme (IDE) or disruption of the axonal transport of the amyloid precursor protein.