for the last __ years, we have assumed that the underlying pathophysiology for Alzheimer’s disease are the neurofibrillary tangles of tau and the amyloid plaques.
current treatment is aimed at increasing amount of acetylcholine in the brain but from what i can tell this is treating the symptoms as opposed to stopping alzheimer’s from the root cause.
a lot of hype has been around lecanemab a monoclonal antibody which binds and gets rid of the plaques, but even this has moderate efficacy. mechanistically this works, but the trial data are not very promising especially with the price tag.
recent research has suggested that alzheimer’s disease can be classed as type 3 diabetes due to its association with metabolic dysfunction, but then goes down the wrong path of functional medicine.