Researchers from the Ludwig Maximilian University (LMU) in Munich discovered a biomarker that's linked to activated neural damage seen in the early stages of Alzheimer's disease. This is the most common form of dementia, which results in problems with memory, thinking and behavior that can interfere with daily tasks.

They found that a concentration of a specific segment of the protein TREM2 in cerebrospinal fluid (CSF) is significantly elevated in the early stages of the health issue. TREM2 is important for the function of specialized cells that protect the body by ingesting harmful foreign bodies, called microglia, which are only found in the brain.

"Our findings indicate that TREM2 plays an important role in the progression of Alzheimer's, and perhaps even other forms of dementia. It appears to be part of a defense mechanism that involves phagocytic cells that eliminate damaged nerve cells and toxic protein deposits, such as those made up of beta-amyloid peptides," said lead study author Christian Haass, who is the Chair of Metabolic Biochemistry at LMU and the speaker of the German Center for Neurodegenerative Diseases (DZNE) in Munich.

During the study, researchers examined over 400 Alzheimer's patients who showed cognitive defects of varying severity to age-matched controls. Findings revealed that patients who showed signs of mild cognitive impairment had higher concentrations of a certain fragment of TREM2. However, amounts detected in patients with advanced Alzheimer's were significantly lower.

"This correlates with the level of activity of the microglial cells, which falls off as the condition progresses. This in turn presumably means that less beta-amyloid and cell debris can be cleared away," Haass said. "We, therefore, believe that this biomarker provides us with a way to assess the capacity of innate immune cells in the brain to degrade and dispose toxic material."

Though researchers are still unclear whether concentration changes of the TREM2 fragment in cerebrospinal fluid causes the progression into Alzheimer's, they believe that an early increase in TREM2 levels can be attributed to the activation of microglia in response to initial signs of damage to nerve cells in the brain.

Alzheimer's disease remains the sixth leading cause of death in the United States and, by 2050, estimates suggest that costs for the health issue could rise as high as $1.1 trillion.

The study is published today in the journal EMBO Molecular Medicine.