Researchers have identified a brain inflammation marker in patients at early asymptomatic stages of Alzheimer's disease.
This molecule may provide clinicians with a rapidly detectable biomarker for the transition from preclinical Alzheimer's disease to cognitive impairment and progression to full dementia.
The study on a large group of human patients showed that the concentration of a specific segment of the protein TREM2 in cerebrospinal fluid (CSF) is significantly elevated in early stages of Alzheimer's disease.
"Our findings indicate that TREM2 plays an important role in the progression of Alzheimer's, and perhaps even other forms of dementia," said lead researcher Christian Haass from the Ludwig Maximilian University of Munich (LMU) in Germany.
"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," Haass noted.
The results of this study were published online in the journal EMBO Molecular Medicine.
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Alzheimer's disease, an increasing problem in today's ageing populations, is characterised by amyloid peptide plaques and tau protein aggregates in nerve cells.
However, the currently available preclinical diagnostics based on amyloid peptide and tau protein forms in the cerebrospinal fluid are not sufficiently specific, as individuals exhibiting them may still retain normal cognitive capabilities for years before developing dementia.
In the present work, the researchers focused on the TREM2 protein, which functions in specialised brain immune cells called microglia that clear toxic material resulting from nerve cell injury.
Microglia are activated during Alzheimer's disease progression and may mediate an initially protective inflammatory response.
Conducting a cross-sectional study of a large cohort of patients with different levels of cognitive impairment and different disease stages, the researchers found that the amounts of a TREM2 fragment in the cerebrospinal fluid were highest during early stages characterised by mild cognitive impairment symptoms.
Its levels declined again in late-stage patients with full dementia, closely mirroring the pattern of microglia activity during the course of the disease, the study said.