Alzheimer’s disease is often called a thief of identity, gradually erasing memory, language, and reasoning until little of the self remains.
But by the time symptoms appear and doctors confirm a diagnosis, the brain has already been irreparably damaged.
No cure exists, and treatments have long fallen short.
Now, new research led by Florida International University neuroscientist Tomás R. Guilarte points to a promising new target that may allow doctors to detect—and potentially intervene against—Alzheimer’s decades before symptoms begin.
The findings, published in Acta Neuropathologica, center on a protein called TSPO, which may serve both as an early biomarker and as a potential pathway to slow or delay the disease.
Most drug development has focused on the well-known hallmarks of Alzheimer’s: sticky amyloid plaques and twisted tangles of tau protein that kill neurons.
But hundreds of clinical trials aimed at removing amyloid or tau have ended in disappointment.
Many scientists now believe that effective treatment will require targeting multiple processes at once, including the brain’s immune response.
That’s where TSPO, short for translocator protein 18 kDa, comes in. Normally found at low levels, TSPO surges during neuroinflammation—an early process that appears to drive Alzheimer’s progression.
“If we can use TSPO to detect it early, it could mean slowing the disease or delaying symptoms by five or six years,” Guilarte said. “That’s five or six years of better quality of life.”
Using advanced imaging technology, Guilarte’s team tracked when and where TSPO first appeared in the brain.
They found that its increase coincided with the earliest formation of amyloid plaques in the subiculum, part of the hippocampus critical for learning and memory. The highest TSPO levels appeared in microglia—immune cells tasked with protecting neurons—that clustered closest to the plaques.
In a mouse model of Alzheimer’s, TSPO was detectable as early as one and a half months of age, equivalent to an 18- to 20-year-old human. Female mice showed higher levels than males, mirroring real-world patterns where two-thirds of Alzheimer’s patients are women.
Memory decline followed months later, as plaques spread and TSPO levels soared. Human brain tissue from patients confirmed the same pattern.
The study drew on rare genetic cases of Alzheimer’s from Medellín and surrounding villages in Colombia, where about 1,200 people carry a hereditary mutation known as the Paisa mutation. These individuals often develop symptoms in their 30s or 40s and die by their 50s. Samples donated by these patients allowed Guilarte’s team to connect early microglial inflammation with the disease’s progression.
Co-author Daniel Martinez-Perez, a doctoral researcher in Guilarte’s group, emphasized that the work builds on the legacy of Dr. Francisco Lopera, a Colombian neurologist who identified the mutation and worked for decades with affected families. Martinez-Perez is now extending the research to late-onset Alzheimer’s, the more common form that strikes in older age.
Although the current study focused on genetic cases, Guilarte is confident the findings apply broadly. “Decades of studying neurodegeneration convince me that neuroinflammation is a key player in both early and late Alzheimer’s,” he said.
The research suggests that spotting TSPO early could eventually give doctors a head start—perhaps years—before symptoms set in. With further study, it may even open the door to therapies that restore microglial balance, slow inflammation, and delay the devastating progression of Alzheimer’s disease.
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