Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Thursday, October 29, 2020

Shared Underlying Pathways Found for Fatigue and Depression in MS

Could this explain the massive fatigue found in stroke survivors? WHOM DO WE ASK THAT FUCKINGLY SIMPLE QUESTION?

Shared Underlying Pathways Found for Fatigue and Depression in MS

Proinflammatory cytokines, tryptophan catabolites, and the gut-brain axis may have key roles in the mechanisms underlying chronic fatigue and symptoms associated with major depressive disorder (MDD) in multiple sclerosis (MS), according to study results published in Multiple Sclerosis and Related Disorders.

Study researchers sought to better understand the relationship between chronic fatigue and depression in MS, as well as their mutual underpinning pathways. To achieve this, they conducted a descriptive review consisting of a summary of findings from several studies in MS and MDD.

The kynurenine pathway (KP) of tryptophan metabolism represents an essential regulator of the production of neurotoxic and neuroprotective compounds. Study researches noted that kynurenine (KYN), as such, which is converted from tryptophan at the initial and rate-limiting step of KP, can cause symptoms of anxiety or depression. Some research suggests that the KP may play a role in the progression of MS, possibly by linking inflammation and excitotoxic neurodegeneration. In other studies, low tryptophan levels and a high KYN/tryptophan ratio were good predictors of depression in patients with MS.

Several studies have also linked gut dysbiosis and increased gut permeability to higher levels of depression and fatigue, particularly in the setting of MS. Additionally, increased gut permeability may be associated with changes in ceramide levels in MS. Ceramides have normally been increased in cases of depression and fatigue.

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Unusual levels of proinflammatory cytokines have also been demonstrated in patients with MS, yet fewer studies have focused on the link between cytokines and depression severity in this population. One study indicated that m-RNA expression of TNF-α and IFN-γ are significantly associated with depression severity during an acute MS attack, whereas another uncovered correlations between IFN-γ production and depression in patients with MS.

According to the authors of the review article, longitudinal studies that measure “immune-inflammatory and KYN pathway biomarkers” are needed to improve “understanding of the underlying pathological mechanisms” associated with chronic fatigue and depression in MS.

Reference

Ormstad H, Simonsen CS, Broch L, Maes M, Anderson G, Celius EG. Chronic fatigue and depression due to multiple sclerosis: Immune-inflammatory pathways, tryptophan catabolites and the gut-brain axis as possible shared pathways. Mult Scler Relat Disord. 2020;46:102533. doi:10.1016/j.msard.2020.102533

 

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