Until the 1990s, it was generally accepted among scientists that amyloid beta (AB), the protein that forms toxic plaques in the brains of Alzheimer’s patients (see Alzheimer’s Disease: A General Overview), only accumulated outside of neurons. This view changed when researchers discovered that AB could also accumulate inside neurons. Later studies suggested that this intracellular AB could kill the neuron and cause it to burst open, releasing the plaques into the brain to potentially kill more cells in a deadly chain reaction. However, it remained unclear exactly how AB was able to kill these neurons from the inside.
A study published in Aging and Mechanisms of Disease suggests an answer to this question and even offers a prospective solution. The researchers observed that when human nerve cells were induced to produce intracellular amyloid beta, the production of immune defense molecules called cytokines was increased. These cytokines initiated an inflammatory reaction that ultimately caused the cell to burst open and die. These results suggest that intracellular AB can kill neurons by essentially tricking the brain’s immune system into attacking itself.
Interestingly, enhancing a specific cannabinoid receptor prevented AB from accumulating in these cells, saving them from the immune system attack. In particular, THC, a cannabinoid that’s found in marijuana, was able to bind the most effectively to this receptor and completely eliminated AB from the cells. These results may explain why mice with genetically-induced Alzheimer’s disease show improved memory when exposed to cannabinoids, though this effect has not yet been confirmed in humans. Future studies plan to test synthetic cannabinoids to see if administering them to people with mild cognitive impairment may prevent the disease from progressing to Alzheimer’s.