If you have read his books, you will be familiar with Dr. Bredesen's different types of AD.
Here we have some molecular research that shows that what actually happens in the brain can be characterized by different gene expression profiles and molecular drivers. The end results show differences in plaque, tangles and neuroinflammation for each type.
"One of these, dubbed type C, fit a classic Alzheimer’s pathological profile, with numerous plaques and tangles as well as neuroinflammation. In types A and B, however, tau pathology predominated, with fewer plaques evident. Type A was distinguished by neuronal hyperexcitability, B by loss of oligodendrocytes. At a more granular level, B and C could be broken down further into two related groups, for a total of five molecular subtypes."
And yes, ApoE status was linked to the different types.
"The scientists subdivided Type C into two subtypes, C1 and C2. At a genetic level, C1 was more likely than the other subtypes to be found in APOE4 carriers; this allele associates with plaque burden and AD risk. Conversely, C2 was not enriched among APOE4 carriers. Overall, this subtype had fewer expression changes than did C1, with Aβ and apoptosis gene pathways the same as in control brain."
This seems like some groundbreaking work, which could be helpful in both creating new diagnostic markers and individualizing treatment plans.
"Researchers agreed on the need for new fluid biomarkers to distinguish subtypes. The current ATN markers of amyloid, tau, and NfL cannot capture the complexity of the disease, Seyfried said. Zhang plans to incorporate peripheral biomarkers and clinical features into the characterization of his subtypes."
Would be interesting to see if this could be mapped to Bredesen's types and treatments.https://www.alzforum.org/news/research- ... alzheimers