Both the cause and treatment of Alzheimer’s are elusive.  Current treatments are modestly effective at best.  Recently touted to be the god-send treatment by removing the amyloid plaque the monoclonal therapy (aducanumab and lecanemab) has been a disappointment.   

In fact, their failure has led to a shift in focus from the amyloid as the prime culprit to mitochondria.  Yes, amyloid deposits are found in the Alzheimer’s brain but so too is found a reduction in mitochondria.  Mitochondria are the powerhouse of neuronal cells (actually all human cells).  Mitochondria generate the glucose that allows optimal neuron activity and reducing its availability impacts cognition. 

But, another factor in the existing mitochondria in Alzheimer’s patients is they have a reduced mitochondria-associated membrane (MAM) electrical function.  Excuse the pun, but current theory for our cognition is the electrical field generated by MAM in our brain cells.  MAMs are the gatekeepers for ion flux which generates the electrical field.  Reduced electrical field leads to neuronal degeneration and loss of cognition.