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, October 26, 2024

Neuroplasticity-related effects of vitamin D relevant to its neuroprotective effects: A narrative review

 Ask your competent? doctor for EXACT PROTOCOLS on how to get synaptogenesis, dendritic branching and axon pathfinding done so you can recover from your stroke. Your doctor better know all about these and how to get the connections done!

Synaptogenesis is the formation of synapses between neurons in the nervous system

Neuroplasticity-related effects of vitamin D relevant to its neuroprotective effects: A narrative review

https://doi.org/10.1016/j.pbb.2024.173899
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Highlights

  • The neuroplasticity-related mechanisms of vitamin D are discussed.
  • The increased expression of neurotrophins and their receptors by vitamin D is reviewed.
  • The modulation of synaptogenesis by vitamin D is provided.
  • The role of vitamin D in depression, Parkinson's and Alzheimer's disease is examined.

Abstract

The pathophysiology of a wide range of central nervous system (CNS) disorders, such as neurodegenerative and psychiatric diseases, has been associated with impairment of neurogenic and synaptogenic processes. Therefore, pharmacological and/or nutritional strategies based on the stimulation and/or restoration of these processes may have beneficial effects against diseases in which these processes are impaired. In this context, vitamin D has emerged as a promising neuroprotective compound. Due to its pleiotropic properties, it can interact with multiple molecular targets and thereby affect different cell types, including neurons and glial cells. This neurosteroid contributes to CNS homeostasis by non-genomic and genomic mechanisms through its interaction with vitamin D receptors (VDRs). Among several properties of this vitamin, its role in neuronal proliferation and differentiation as well as in synaptic plasticity has received attention. Considering this background, this narrative review aims to highlight the neuroplasticity-related mechanisms of vitamin D that may be associated with its neuroprotective effects.(What are the amounts?)

Introduction

The mechanisms regulated by vitamin D are not limited to its involvement in the regulation of bone metabolism and calcium homeostasis. Its role in cell differentiation and immune system function has been extensively studied. In addition, the role of vitamin D in brain development and function has attracted particular interest in recent decades (Kesby et al., 2011; Cui and Eyles, 2022). Evidence suggests that vitamin D is a pleiotropic molecule capable of interacting directly with multiple targets (Kouba et al., 2024), a property that may be related to its effects on cell differentiation (Ko et al., 2004), neurotrophin expression (Féron et al., 2005), intracellular calcium signaling (Brewer et al., 2006), neurotransmitter release and synthesis (Kesby et al., 2017), and anti-inflammatory and antioxidant pathways (McCann and Ames, 2008; Cui et al., 2019). Therefore, hypovitaminosis D impairs the expression of several molecular targets involved in these cellular events (DeLuca et al., 2013; Kouba et al., 2022).
The prominent role of vitamin D in central nervous system (CNS) homeostasis suggests that deficiency of this vitamin may also be associated with a variety of brain disorders. Indeed, studies have reported an association between hypovitaminosis D and an increased risk of Azheimer's disease (Annweiler et al., 2013), Parkinson's disease (Ogura et al., 2021), and major depressive disorder (MDD) (Parker et al., 2017) in adults. In addition, vitamin D has been shown to improve the symptoms and behavioral changes associated with these disorders and may be used as a therapeutic adjuvant and/or potential neuroprotective agent (Kouba et al., 2022, Kouba et al., 2023b; Pignolo et al., 2022). Given that Parkinson's disease, Alzheimer's disease, and MDD are associated with impairment of neurogenic and synaptogenic processes (Skaper et al., 2017; Levy et al., 2018; Zhang and Lu, 2021), this narrative review aims to highlight neuroplasticity-related mechanisms of vitamin D that may be associated with its neuroprotective effects.(What are the amounts?)

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