By Dale Bredesen, M.D., Chief Science Officer for Apollo Health

We have all been participating in a revolution, moving Alzheimer’s from ineluctable to preventable and in many cases reversible, so that ultimately Alzheimer’s will be a rare cause of dementia. The therapeutic approach we originated in 2012 continues to evolve as we perform clinical trials and gather data from thousands of people who have utilized PreCODE or ReCODE, and the latest development, which we have included in our new clinical trial, is to include new blood tests that provide an ongoing look at whether the brain is responding to the protocol. These should be instrumental in guiding us to optimize the approach for each person. 

● The first is phospho-tau 181 (p-tau 181), which measures a molecule that normally stabilizes the processes (axons) protruding from neurons (like bolts to stabilize a rafter), but when phosphorylated, falls off, stops stabilizing, and allows the processes to collapse. Thus the higher the p-tau 181, the more synaptoclastic activity is ongoing, so we’d like to reduce the p-tau 181, which takes several months. A related marker, p-tau 217 (181 and 217 refer to the site on the tau that is phosphorylated, and these two sites are specific for Alzheimer’s), may ultimately replace p-tau 181 because it is more sensitive to early changes, but it is not yet clinically available.

Abeta 42:40 ratio is another new blood test, and this reflects amyloid deposition in the brain, with a reduced 42:40 ratio correlating with increased brain deposition. This is included, along with age and ApoE status, in a probability score for Alzheimer’s.

Neurofilament light (NfL) reflects neuronal damage, but is not specific for Alzheimer’s since it may also be elevated in other neurodegenerative diseases such as ALS. 

Glial fibrillary acidic protein (GFAP) is a marker of the activation of astrocytes, the glial cells that support the neurons. The advantage of this test is that, although it is not specific for Alzheimer’s, it is a sensitive measure of damage that is increased earlier than other markers, thus helpful as an early warning in any brain-related pathology, from Alzheimer’s to frontotemporal dementia to chronic traumatic encephalopathy (CTE).

These tests thus offer complementary information, informing us about the status of the brain, whether there is ongoing neuronal damage, amyloid deposition, early changes of concern, and whether the personalized protocol is leading in a promising direction for any patient or whether it should be modified. These tests should therefore lead to continued optimization of the ReCODE Protocol™, and better outcomes for all.

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