New Clues for Optimized Treatment

When you do not know what is causing a disease or how to treat it, a good first step is to look at the tissue pathology, so you can see the microscopic changes that have occurred.  From the early 1800s to the early 1900s, the pathology of the major neurodegenerative diseases was described. Indeed, all of our major neurodegenerative diseases — from Alzheimer’s to Parkinson’s to Lewy body dementia to Lou Gehrig’s disease, and on and on — have since that time been defined by their pathology. Unfortunately, this does not tell us what is causing the diseases or what to do to treat them effectively. However, we have clues from genetics, epidemiology, and biochemistry that have taught us enough to be able to prevent and reverse cognitive decline for many people. As new clues appear, we can refine and enhance the precision medicine approach we developed, which continues to prove effective.

A fascinating study has just appeared that fits beautifully with the notion that one common driver of neurodegeneration is infections: a gene that is mutated in some cases of Parkinson’s, called LRRK-2, turns out to reduce the ability of cells to kill the tuberculosis organism, called Mycobacterium, and potentially other bacteria, as well. This fits nicely with the increased production of alpha-synuclein in Parkinson’s since this is a protein that kills bacteria (just like the amyloid peptide that collects in Alzheimer’s disease kills bacteria) and thus could offset the failure associated with the mutated LRRK-2. Studies like this one offer us new clues about why diseases like Alzheimer’s and Parkinson’s occur and how we can more effectively treat them and prevent them. These diseases are destined to become scourges of the past.