Summary: A new study suggests THC, the main psychoactive compound in cannabis, may slow cognitive decline experienced by many people living with HIV.
Source: Michigan State University.
Researchers at Michigan State University report that tetrahydrocannabinol (THC) — a primary compound in marijuana — may help slow the cognitive decline that affects up to half of people living with HIV.
“Many people with HIV experience reduced cognitive function, in part because of chronic inflammation in the brain,” said Norbert Kaminski, lead author of the study published in the journal AIDS. “The immune system remains persistently activated as it fights the virus, and that ongoing activation appears to damage brain function over time.”
Kaminski and co-author Mike Rizzo, a graduate student in toxicology, found that cannabis compounds can act as anti-inflammatory agents. Their experiments showed reduced numbers of a specific inflammatory white blood cell type, known as CD16+ monocytes, and decreased levels of inflammatory signaling proteins released by these cells.
“Lowering the number and activity of these inflammatory cells could slow—or possibly halt—the cascade of inflammation that contributes to cognitive decline,” Rizzo said. “That could help people with HIV preserve cognitive abilities longer.”
For the study, the researchers collected blood samples from 40 people living with HIV who reported either using or not using marijuana. They isolated white blood cells from each donor and measured inflammatory cell populations and inflammatory protein levels, then tested how THC influenced those cells in laboratory conditions.
“Participants who did not use cannabis showed substantially higher levels of inflammatory monocytes compared with those who did use cannabis,” Kaminski said. “Remarkably, the monocyte and inflammatory marker levels in cannabis users were closer to those typically seen in HIV-negative, healthy individuals.”
Kaminski, director of MSU’s Institute for Integrative Toxicology, has studied cannabis and the immune system since 1990. His lab was among the first to identify receptors on immune cells that bind cannabinoids, clarifying how cannabis-derived compounds directly influence immune cell behavior.
HIV (human immunodeficiency virus) infects cells of the immune system and can alter or destroy their normal functions. Modern antiretroviral therapy helps preserve immune cell populations and control viral replication, but some immune cells can remain chronically activated and promote inflammation despite treatment.

“We will continue to study how these immune cells interact and drive inflammation in the brain,” Rizzo said. “Insights from this work may also be relevant to other neurodegenerative conditions, such as Alzheimer’s and Parkinson’s disease, where similar inflammatory cells have been implicated.”
The researchers emphasize that the beneficial effects observed in the study do not necessarily mean smoking marijuana is the optimal medical approach. “Future therapies may harness key cannabis-derived compounds in more controlled forms — for example, in a pill or other pharmaceutical formulations — to target inflammation without the risks associated with smoking,” Kaminski said.
Source: Michigan State University
Publisher: Neuroscience News (coverage of academic research)
Image Source: NeuroscienceNews.com image (public domain)
Original Research: Rizzo, M. D.; Crawford, R. B.; Henriquez, J. E.; Aldhamen, Y.; Gulick, P.; Amalfitano, A.; Kaminski, N. E. “HIV-infected cannabis users have lower circulating CD16+ monocytes and IP-10 levels compared to non-using HIV patients.” Published online November 30, 2017. DOI: 10.1097/QAD.0000000000001704
Recommended citation example: Michigan State University. “Marijuana May Help People with HIV Preserve Cognitive Function.” Neuroscience News, December 2017.
Abstract
HIV-infected cannabis users have lower circulating CD16+ monocytes and IP-10 levels compared to non-using HIV patients
Objective:
Chronic immune activation and elevated numbers of circulating CD16+ monocytes are linked to HIV-associated neuroinflammation. The study compared circulating CD16+ monocyte levels and interferon-γ-inducible protein 10 (IP-10) between HIV-positive cannabis users and non-users, and tested whether in vitro exposure to Δ9-tetrahydrocannabinol (THC) altered CD16 expression or IP-10 production by monocytes.
Design:
The research measured circulating CD16+ monocytes and serum IP-10 in HIV-positive cannabis users and non-users. In vitro experiments exposed primary leukocytes from HIV-negative and HIV-positive donors (both cannabis users and non-users) to THC to determine its impact on monocyte phenotype and inflammatory protein production.
Methods:
Flow cytometry quantified circulating CD16+ monocytes and serum IP-10 in donor samples. Peripheral blood mononuclear cells (PBMCs) from HIV-negative and HIV-positive donors were treated in vitro with THC and interferon-α to assess effects on CD16 induction and IP-10 secretion.
Results:
HIV-positive cannabis users had lower levels of circulating CD16+ monocytes and reduced serum IP-10 compared with HIV-positive non-users. Monocytes from cannabis users were less able to upregulate CD16 in response to interferon-α in vitro, while cells from HIV-negative and HIV-positive non-users showed robust CD16 induction. In vitro THC treatment reduced the transition of CD16− monocytes to CD16+ and lowered monocyte-derived IP-10 production.
Conclusions:
Components of cannabis, including THC, appear to slow peripheral monocyte processes associated with HIV-related neuroinflammation. These anti-inflammatory effects may contribute to reduced neuroinflammatory signaling and could help explain observed differences in cognitive outcomes among people living with HIV who use cannabis.