A new study offers hope for earlier Alzheimer’s detection and intervention. Researchers found that TSPO, a brain inflammation biomarker, could identify the disease years before symptoms emerge, potentially transforming diagnosis and treatment approaches.
A groundbreaking study by researchers at Florida International University has identified a biomarker that could revolutionize the way Alzheimer’s disease is diagnosed and treated. The biomarker, TSPO (translocator protein 18 kDa), was found to indicate brain inflammation and could help detect Alzheimer’s years before significant memory loss and other symptoms manifest.
“This is the first study to really examine how early this biomarker increases and where it begins rising in the brain,” lead researcher Tomás R. Guilarte, the dean of FIU’s Robert Stempel College of Public Health & Social Work, said in a news release. “If we can use this information to help delay Alzheimer’s progression by even five years, it can drastically improve patients’ lives and reduce disease prevalence.”
The study, published in the journal Acta Neuropathologica, utilized advanced imaging software to track TSPO levels in genetically modified mouse models of familial Alzheimer’s. These findings were corroborated using human brain tissue donated by families from Antioquia, Colombia.
These families carry the “paisa” mutation and are part of the largest known group of individuals with early-onset familial Alzheimer’s, first identified by the late Francisco Lopera, a co-author of the study.
For individuals with this mutation, symptoms usually appear in their 30s or 40s, and they typically die in their 50s.
In the mouse models, the researchers discovered elevated TSPO levels in the subiculum — a critical part of the hippocampus — as early as six weeks of age. This timeline is roughly equivalent to age 18–20 in humans.
Significantly higher levels of TSPO were found in microglia, the brain’s immune cells, especially those near amyloid plaques. Female mice displayed even higher TSPO levels, reflecting the fact that two-thirds of Alzheimer’s patients are women.
The brain tissue samples from the Colombian patients carrying the paisa mutation exhibited a similar pattern. Even in advanced stages of Alzheimer’s, TSPO levels remained elevated in microglia near plaques. These findings prompt new questions about the role of TSPO — does it contribute to damage or help protect the brain? And could modulating TSPO, either by blocking or enhancing it, potentially slow down disease progression?
The research team is now exploring these questions using a specialized Alzheimer’s mouse model that lacks TSPO. They are also broadening their research to include sporadic, late-onset Alzheimer’s cases, which make up over 90% of all diagnoses.
“The more we understand these processes,” added first author Daniel Martínez Pérez, a doctoral candidate in Guilarte’s lab, “the closer we get to tailoring treatments that can truly help — before it’s too late.”
Source: Florida Atlantic University