When immune systems go awry, they can wreak havoc, triggering everything from diabetes to – scientists now believe – Alzheimer’s disease (AD). But immune systems are supposed to protect, not injure, the body. So what if scientists could pinpoint a window before things go amiss and harness the defense system in a way that curbs or prevents AD from taking hold?
Glossary of termsAmyloid: Sticky protein aggregates that build up, becoming plaques in the brains of people with AD. APOE ε4: The apolipoprotein E gene is involved in making a protein that helps carry cholesterol and other types of fat in the bloodstream. Problems in this process are thought to contribute to the development of AD. The APOE ε4 allele is associated with greater risk for Alzheimer’s disease. Biomarker: A measurable marker in the body that indicates a disease, infection or environmental exposure. Glia: Non-neuronal cells, including astrocytes, in the nervous system. Neurons: Nerve cells in the brain and spinal cord. Tau: A protein that forms insoluble filaments that accumulate as neurofibrillary tangles in AD.
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It’s one possibility being targeted by a group of University of Colorado Anschutz Medical Campus researchers bent on halting the brain-destroying disease that affects 6.7 million Americans 65 or older.
In a recently published study, the group found an association between higher levels of an immune system-related biomarker and decreased microstructure in parts of the brain highly vulnerable to AD. The finding, which signals a greater risk of cognitive difficulties, was distinctly higher in women.
Finding mostly seen in women
“We were surprised at how strong the effect was,” said Brianne Bettcher, PhD, a clinical researcher at the University of Colorado Alzheimer's and Cognition Center (CUACC), who looked with colleagues at a biomarker called GFAP (glial fibrillary acidic protein), an important protein believed to be released with central nervous system (CNS) injuries, such as stroke or brain injuries.
“It was pretty notable, and it was mostly seen in women.”
Knowing that women are at almost twice the risk of AD as men, the scientists looked for the difference, but were still surprised by the wide sex gap as well as the findings overall, Bettcher said. “That means these helper cells (astrocytes that release GFAP) are really critical and probably impacting Alzheimer’s disease from an early, early stage.”
“I think another take-away from it is that we need to be focusing more on why
there are these sex differences in risk for Alzheimer’s disease. We should not accept
that women are at greater risk.” – Brianne Bettcher, PhD
The study sample of 109 (out of 114) participants included healthy older adults and adults with symptomatic AD identified from the CUACC Bio-AD study database. Participants were on average 70 years old, with 44% of individuals having at least one AD-related APOE E4 allele. Females comprised 63.3% of the sample.
Bettcher, an associate professor in the departments of Neurology and Neurosurgery at the CU School of Medicine, focuses largely on the neurobiology of aging and understanding the role of immune system dysfunction in aging and AD. The finding could help open the latch to that therapeutic window she seeks.
“My real passion is trying to understand before symptoms even begin what is putting someone down a path that could lead to Alzheimer’s disease and how we could potentially avoid that,” said Bettcher, who talks more about the study in the condensed Q&A below.
