Any thoughts on whether Trontinemab would work work differently for APOE4/4 if there is evidence of mild chronic microangiopathy and vascular calcifications in the anterior and posterior circulate. I am trying to help my sister decide if this is the best clinical trial to enter into and feel strongly that the benefit/risk analysis does not suggest that it is. Not sure that clearing the amyloid plaques will result in actual cognitive benefit if not targeting vascular issues. I can't find actual data on side effects for Aria-H for the trial. Are there any trials that are combining targets? She is very scared that she is nearing a "tipping point" in the progression of the disease which is what she is being told by the trial and that it is important to begin trials before then. (Currently plasma Tau positive but Tau Pet neg and amyloid pet positive with minimal cognitive issues) Are there any defining cutoffs for efficacy? Thank you.
Regarding the appreciation for neuroinflammation and neurodegeneration: Would you expect to see autonomic nervous system dysfunction/failure earlier in disease?
Dear Amy, in classic AD, you do not see autonomic system failure early in the disease. However, a small brain area called the locus coeruleus begins to malfunction very early, sometimes many years before memory problems appear. This region helps control attention, alertness, sleep, and stress responses by releasing a chemical called norepinephrine that supports communication between brain cells and helps protect the brain from inflammation. tau starts to build up in these cells, causing them to weaken or die. Because the locus coeruleus connects to many parts of the brain, its early damage may contribute to problems like sleep changes, mood symptoms, and difficulty focusing, and may also help the disease spread to areas involved in memory. But sometimes these changes are subtle.
Any thoughts on whether Trontinemab would work work differently for APOE4/4 if there is evidence of mild chronic microangiopathy and vascular calcifications in the anterior and posterior circulate. I am trying to help my sister decide if this is the best clinical trial to enter into and feel strongly that the benefit/risk analysis does not suggest that it is. Not sure that clearing the amyloid plaques will result in actual cognitive benefit if not targeting vascular issues. I can't find actual data on side effects for Aria-H for the trial. Are there any trials that are combining targets? She is very scared that she is nearing a "tipping point" in the progression of the disease which is what she is being told by the trial and that it is important to begin trials before then. (Currently plasma Tau positive but Tau Pet neg and amyloid pet positive with minimal cognitive issues) Are there any defining cutoffs for efficacy? Thank you.
Pam (3/4)
Dear Pam, thank you for reaching out. I would suggest a thoughtful discussion with the neurologist about the risks and benefits of such treatments.
Regarding the appreciation for neuroinflammation and neurodegeneration: Would you expect to see autonomic nervous system dysfunction/failure earlier in disease?
Dear Amy, in classic AD, you do not see autonomic system failure early in the disease. However, a small brain area called the locus coeruleus begins to malfunction very early, sometimes many years before memory problems appear. This region helps control attention, alertness, sleep, and stress responses by releasing a chemical called norepinephrine that supports communication between brain cells and helps protect the brain from inflammation. tau starts to build up in these cells, causing them to weaken or die. Because the locus coeruleus connects to many parts of the brain, its early damage may contribute to problems like sleep changes, mood symptoms, and difficulty focusing, and may also help the disease spread to areas involved in memory. But sometimes these changes are subtle.