Researchers have identified TREM2 as a target to potentially enhance the ability of immune cells in the brain to remove amyloid beta, solid deposits of misfolded proteins associated with the progression of Alzheimer’s disease. Removal of amyloid beta remains the primary focus of the Alzheimer’s research community, despite the continued lack of progress towards working therapies based on this approach. An increasing number of researchers are investigating alternatives to the existing approaches to amyloid immunotherapy, so far failing to achieve meaningful results in human trials.
The slow accumulation of amyloid beta and other metabolic waste in the brain looks a lot like the consequence of a slow failure of clearance mechanisms, as amyloid levels are actually quite dynamic from moment to moment. One candidate for this failure is the age-related deterioration of immune activity, in and of itself a very complex topic – which is one reason to think that therapies based on improved immune function might be helpful. Other candidates include failure of filtration of cerebrospinal fluid in the choroid plexus, or more recent views on the failure of cerebrospinal fluid drainage. Alzheimer’s is a complex condition, and the brain is a complex
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