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, June 20, 2024

The Moderating Effect of Serum Vitamin D on the Relationship Between Beta-Amyloid Deposition and Neurodegeneration

Useless. You descried a problem, did nothing to specify how to counteract low vitamin D levels; supplements or food and the amounts needed! And then you lazily threw out the further research needed canard, knowing that with NO stroke leadership nothing will occur.

 The Moderating Effect of Serum Vitamin D on the Relationship Between Beta-Amyloid Deposition and Neurodegeneration

Junha Park 1, 2, Min Soo Byun 1, 2, 3*, Dahyun Yi 4, Hyejin Ahn 5, Joon Hyung Jung 6, Nayeong Kong 7, Yoon Young Chang 1, 2, Gijung Jung 4, Jun-Young Lee 1, 8, Yu Kyeong Kim 9, 10, Yun-Sang Lee 10, Koung Mi Kang 11, Chul-Ho Sohn 11, Dong Young Lee 1, 2, 3
1Department of Psychiatry, Seoul National University College of Medicine, Seoul, Republic of Korea , 2Department of Neuropsychiatry, Seoul National University Hospital, Seoul, Republic of Korea , 3Seoul National University Dementia Research Center, Seoul, Republic of Korea , 4Institute of Human Behavioral Medicine, Seoul National University Medical Research Center, Seoul, Republic of Korea, 5Interdisciplinary program of cognitive science, Seoul National University College of Humanities, Seoul, Republic of Korea, 6Department of Psychiatry, Chungbuk National University Hospital, Cheongju, Republic of Korea, 7Department of Psychiatry, Keimyung University Dongsan Medical Center, Daegu, Republic of Korea, 8Department of Neuropsychiatry, SMG-SNU Boramae Medical Center, Seoul, Republic of Korea, 9Department of Nuclear Medicine, SMG-SNU Boramae Medical Center, Seoul, Republic of Korea, 10Department of Nuclear Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea , 11Department of Radiology, Seoul National University Hospital and Seoul National University College of Medicine, Seoul, Republic of Korea
Received: March 16, 2024; Revised: June 1, 2024; Accepted: June 9, 2024; Published online: June 9, 2024.
© The Korean College of Neuropsychopharmacology. All rights reserved.


Abstract

Objective: 
 
 Previous studies have reported that vitamin D deficiency increased the risk of Alzheimer’s disease (AD) dementia in older adults. However, little is known about how vitamin D is involved in the pathophysiology of AD. Thus, this study aimed to examine the association and interaction of serum vitamin D levels with in vivo AD pathologies including cerebral beta-amyloid (Aβ) deposition and neurodegeneration in nondemented older adults.
 
Methods: 
428 nondemented older adults were recruited from the Korean Brain Aging Study for the Early Diagnosis and Prediction of Alzheimer’s Disease, a prospective cohort that began in 2014. All participants underwent comprehensive clinical assessments, measurement of serum 25-hydroxyvitamin D (25[OH]D), and multimodal brain imaging including Pittsburgh compound-B (PiB) positron emission tomography and magnetic resonance imaging. Global PiB deposition was measured for the Aβ biomarker. Intracranial volume-adjusted hippocampal volume (HVa) was used as a neurodegeneration biomarker.
 
Results: 
Overall, serum 25(OH)D level was not associated with either Aβ deposition or HVa after controlling for age, sex, apolipoprotein E ε4 positivity, and vascular risk factors. However, serum 25(OH)D level had a significant moderation effect on the association between Aβ and neurodegeneration, with lower serum 25(OH)D level significantly exacerbating cerebral Aβ-associated hippocampal volume loss (β = 34.612, p = 0.008).
 
Discussion: 
 
Our findings indicate that lower serum vitamin D levels may contribute to AD by exacerbating Aβ-associated neurodegeneration in nondemented older adults. Further studies to explore the potential therapeutic effect of vitamin D supplementation on the progression of AD pathology will be necessary.

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