CELS contrasting enhancing lesions also known as gadliolinium enhancing lesions. These are not slowly expanding lesions = SELS. But disease activity reduces as you get older. So something to look forward too:-). However we have known this for years. Your immune system ages as we get older and is one of the reasons we see more cancers in older age.
How does it inform trials? It says if you have older people in trials and you are looking for activity it will be harder to see a difference meaning a longer trial or needs a bigger trial..so do you exclude people from trials due to age?..
It always happens, chariotMS is unusual in this respect .
The problem then is no evidence is collected that says the agent will work in the demographics.so does it restrict access. There are plenty of papers reporting more limited effects of agents in people aged below 55.
However as people are dying with active lesions there is biology that can be modified.
Strijbis EM, Coerver E, Mostert J, van Kempen ZLE, Killestein J, Comtois J, Repovic P, Bowen JD, Cutter G, Koch M. Association of age and inflammatory disease activity in the pivotal natalizumab clinical trials in relapsing-remitting multiple sclerosis. J Neurol Neurosurg Psychiatry. 2023:jnnp-2022-330887. doi: 10.1136/jnnp-2022-330887.
Background: Focal inflammatory disease activity in relapsing-remitting multiple sclerosis (RRMS) diminishes with increasing age. Here we use patient-level data from randomised controlled trials (RCTs) of natalizumab treatment in RRMS to investigate the association of age and inflammatory disease activity.
Methods: We used patient-level data from the AFFIRM (natalizumab vs placebo in relapsing-remitting MS, NCT00027300) and SENTINEL (natalizumab plus interferon beta vs interferon beta in relapsing remitting MS, NCT00030966) RCTs. We determined the proportion of participants developing new T2 lesions, contrast-enhancing lesions (CELs) and relapses over 2 years of follow-up as a function of age, and investigated the association of age with time to first relapse using time-to-event analyses.
Results: At baseline, there were no differences between age groups in T2 lesion volume and number of relapses in the year before inclusion. In SENTINEL, older participants had a significantly lower number of CELs. During both trials, the number of new CELs and the proportion of participants developing new CELs were significantly lower in older age groups. The number of new T2 lesions and the proportion of participants with any radiological disease activity during follow-up were also lower in older age groups, especially in the control arms.
Conclusions: Older age is associated with a lower prevalence and degree of focal inflammatory disease activity in treated and untreated RRMS. Our findings inform the design of RCTs, and suggest that patient age should be taken into consideration when deciding on immunomodulatory treatment in RRMS.
How much neurodegeneration process is secondary to damage from relapses?
A. If it is not secondary then older age we will see more neurodegen and less inflammation doesnt mean much to a MSer .
B. If there are large portion of the neurodegen process is secondary to something DMT can control is what we all want to hear.
Prof G is making it to sound more like A, while older view is more B, what’s your view?
Is this reduction in CELS and slowing of new activity only seen in RRMS? What happens in SPMS?
My neurologist recently told me MS stops after the age of 60???
Maybe you need a new neurologist.