A protein involved in Alzheimer's disease (AD) may be a promising target for treating neurological disorders in human immunodeficiency virus (HIV) patients, suggests a study published in JNeurosci of rat neurons and brain tissue from deceased humans. The research shows that the two conditions may damage neurons in similar ways.
Although HIV-associated neurological disorders (HAND) and AD have symptoms in common, whether they also share underlying mechanisms of disease progression is controversial because HAND patients do not exhibit the amyloid plaques that are characteristic of AD. To address this question, Kelly Jordan-Sciutto and colleagues investigated the role of a well-known AD protein -- β-site amyloid precursor protein cleaving enzyme 1 (BACE1) -- in HAND. The researchers found elevated levels of BACE1 and Aβ oligomers -- the compound thought to be responsible for neuronal damage in AD -- in postmortem brain tissue of HIV-positive humans. Treating rat neurons with HIV-infected white blood cells from healthy humans revealed similar mechanisms of neurotoxicity.
Article: BACE1 mediates HIV-associated and excitotoxic neuronal damage through an APP-dependent mechanism
Corresponding author: Kelly Jordan-Sciutto (University of Pennsylvania, Philadelphia, USA), firstname.lastname@example.org
JNeurosci, the Society for Neuroscience's first journal, was launched in 1981 as a means to communicate the findings of the highest quality neuroscience research to the growing field. Today, the journal remains committed to publishing cutting-edge neuroscience that will have an immediate and lasting scientific impact, while responding to authors' changing publishing needs, representing breadth of the field and diversity in authorship.
About The Society for Neuroscience
The Society for Neuroscience is the world's largest organization of scientists and physicians devoted to understanding the brain and nervous system. The nonprofit organization, founded in 1969, now has nearly 37,000 members in more than 90 countries and over 130 chapters worldwide.