Review from Lassman. It includes "vascular comorbidities" influence.

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frodo
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Review from Lassman. It includes "vascular comorbidities" influence.

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Hans Lassman is one of the heavy weights in research. He has recently written this.

https://www.uni-muenster.de/Ejournals/i ... /3166/3147

8) How do vascular comorbidities influence multiple sclerosis patients?

Clinical epidemiology of MS has shown that patients with vascular risk factors, such as diabetes, hypercholesterolaemia, hypertension, or heart disease have a more aggressive disability progression in comparison to patients lacking these co-morbidities (Marrie et al. 2010). This is also reflected by lower brain volumes (Pichler et al. 2019).

Furthermore, persistence of inflammatory demyelinating lesions and higher lesion volumes are present in brain areas with a blood perfusion that is lower than in other brain areas (Haider et al. 2016). Such a synergism in neurodegeneration may in part be explained by shared effector mechanisms of tissue injury between vascular and inflammatory diseases, including microglia activation, oxidative injury, and mitochondrial damage (Zrzavy et al. 2017, 2018, Mahad et al. 2015).

A strategically important piece in the puzzle of vascular comorbidities and MS, which was missing so far, was the lack of a comprehensive neuropathological description of systemic and intracranial vascular pathology in patients versus controls.

This information has now been provided by a study, which is based on a unique archival collection of MS and control autopsy cases, where detailed information regarding systemic vascular diseases was recorded, and which was collected prior to the availability of disease modifying treatments.

The study shows, as expected, that systemic and intracranial vascular abnormalities increase with age in both the MS and the control group. Young MS patients appear to have a moderate reduction of systemic vascular co-morbidities compared to controls, but this difference disappears with aging.

Within the central nervous system, MS patients showed a profound increase in small arteries with increased perivascular space, perivascular hemosiderin depositions and periarteriolar accumulation of inflammatory cells, a type of pathology which correlated in its extent with the degree of MS-related pathology.

These results underline the presence of age-related vascular co-morbidities in the brain of MS patients, which may be an amplification factor for neurodegeneration and disease progression in aging patients.

Additionally, they indicate that, in contrast to the current view, vascular pathology is not restricted to veins but also affects small arteries, and this arterial pathology develops at least in part independently from systemic vascular risk factors. In particular, the mechanisms how inflammatory infiltrates accumulate around arteries in the MS brain requires further attention.
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