Alzheimer’s is one of the fastest-growing global health problems today (read more about the prevalence rates in a past blog). Up until now, most research and clinical trials have focused on amyloid plaques. Just over a month ago, however, a study published in the Journal of Neuroscience identified a new potential culprit in the development of Alzheimer’s and other neurological disorders: the protein C1q.
C1q attaches itself to pathogens like bacteria or to dead or dying cells in the body, initiating what is called the “complement cascade” where a series of immune-response proteins accumulate on the foreign body or cell, targeting it for destruction. In infants, the complement cascade plays a significant role in brain development by pruning excess synapses (i.e., the structures that facilitate communication between neurons) to improve function efficiency.
In this new study, Stanford University School of Medicine researchers found that in both mouse and human brain tissue, C1q accumulates on synapses as a function of normal brain aging. In some cases, there was as much as a 300-fold age-related buildup. Though the elevated C1q concentrations alone do not trigger synaptic destruction, they do impair communication between neurons, which can in turn interfere with cognitive functions. In addition, the buildup marks these synapses as primary targets if and when immune cells are triggered by a catalytic event such as a brain trauma, systemic infection or series of small strokes. The researchers hope that further study will provide additional evidence for the role of C1q in neurodegenerative diseases and reveal potential intervention paths.
As Partners of the Alzheimer’s Early Detection Alliance (AEDA), San Francisco Home Care Assistance makes community education around the disease a priority. For additional resources or to learn more about how our San Francisco caregivers can support cognitive health through mental stimulation, call us today.