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.

Saturday, January 18, 2025

White matter aging and its impact on brain function

 You competent? doctor has known of myelin problems from your stroke a long time ago, was anything done to solve it? NO? So, pure incompetence in action!

(My doctor told me I had a bunch of white matter hyperintensities but never showed me them on any scan, so I don't know the size, location or any intervention needed, because my doctor knew nothing and did nothing.)

  • demyelinating (23 posts to May 2012)
  • demyelination (7 posts to November 2021)
  • White matter aging and its impact on brain function

    Cover Image - Neuron, Volume 113, Issue 1

    Summary

    Aging has a detrimental impact on white matter, resulting in reduced volume, compromised structural integrity of myelinated axons, and an increase in white matter hyperintensities. These changes are closely linked to cognitive decline and neurological disabilities. The deterioration of myelin and its diminished ability to regenerate as we age further contribute to the progression of neurodegenerative disorders. Understanding these changes is crucial for devising effective disease prevention strategies. Here, we will discuss the structural alterations in white matter that occur with aging and examine the cellular and molecular mechanisms driving these aging-related transformations. We highlight how the progressive disruption of white matter may initiate a self-perpetuating cycle of inflammation and neural damage.

    Keywords

    1. aging
    2. white matter
    3. myelin
    4. neuroinflammation

    Introduction

    In his pioneering work, De Humani Corporis Fabrica (1543), Renaissance anatomist Andreas Vesalius provided one of the earliest descriptions of white matter structure, noting the corpus callosum as a whitish substance distinct from the softer, yellowish cerebrum. Although Vesalius recognized that the corpus callosum connected the two hemispheres, he did not understand that its fibers originated from nerve cell bodies. At the time, white matter was believed to be composed of excretory ducts filled with a “spongy substance” and was thought to be the center of spirit and imagination. Now, we know that white matter primarily consists of myelinated axons, glial cells, blood vessels, and extracellular matrix. Oligodendrocytes, the main cells in white matter, produce myelin sheaths that are crucial for fast signal transmission and for maintaining the functional and structural integrity of axons., Because white matter largely lacks neuronal cell bodies and mainly serves to connect different gray matter areas, it has not received as much as attention as the cortical areas of the brain. Yet, its significance becomes evident when looking at its evolution in primates. Unlike neocortical gray matter, which grows in direct proportion to brain size, white matter mass has increased at a much higher rate, highlighting the crucial role of enhanced connectivity for higher brain function. Consequently, the proportion of white matter in the human brain has risen to about 40%, with myelinated axons being a major component. However, this expansion of white matter also introduces risks, providing a surface for diseases and the effects of aging. As we age, our white matter undergoes several changes. It experiences a reduction in overall volume and exhibits a decline in its microstructural integrity, and there is an accumulation of focal lesions, contributing to a decline in cognitive functions and to the risk for age-related neurological diseases, including dementia and stroke.,,, Many of these changes follow non-linear kinetics, starting slowly and then accelerating at a certain age. In this context, we explore the structural changes in white matter associated with aging and investigate the cellular and molecular mechanisms underlying these age-related transformations. We hypothesize that chronic inflammation and vascular changes are closely linked to the degeneration of myelin and axons with age.

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