Assessing the Impact of Factors that Influence the Ketogenic Response to Varying Doses of Medium Chain Triglyceride (MCT) Oil

2020 ◽  
pp. 1-10
Author(s):  
A.G. Juby ◽  
D.R. Brocks ◽  
D.A. Jay ◽  
C.M.J. Davis ◽  
D.R. Mager
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Healthy Subjects ◽  
Medium Chain Triglyceride ◽  
Nutrient Content ◽  
Individual Variability ◽  
Time Curve ◽  
Medium Chain ◽  
Waist Hip Ratio ◽  
The Impact

Objectives, Design, Setting: The ketogenic effect of medium chain triglyceride (MCT) oil offers potential for Alzheimer’s disease prevention and treatment. Limited literature suggests a linear B-hyroxybutyrate (BHB) response to increasing MCT doses. This pharmacokinetic study evaluates factors affecting BHB response in three subject groups. Participants: Healthy subjects without cognitive deficits <65years, similarly healthy subjects >=65years, and those with Alzheimer’s Disease were assessed. Intervention: Different doses (0g,14g, 28g, 42g) of MCT oil (99.3% C8:0) were administered, followed by fasting during the study period. Measurements: BHB measured by finger prick sampling hourly for 5 hours after ingestion. Each subject attended four different days for each ascending dose. Data was also collected on body composition, BMI, waist/hip ratio, grip strength, gait speed, nutrient content of pre-study breakfast and side effects. Results: Twenty-five participants: eight healthy; average age of 44yr (25-61), nine healthy; 79yr (65-90) and eight with AD; 78.6yr (57-86) respectively. Compiled data showed the expected linear dose response relationship. No group differences, with baseline corrected area under the blood vs. time curve (r2=0.98) and maximum concentrations (r2=0.97). However, there was notable individual variability in maximum BHB response (42g dose: 0.4 -2.1mM), and time to reach maximum BHB response both, within and between individuals. Variability was unrelated to age, sex, sarcopenic or AD status. Visceral fat, BMI, waist/hip ratio and pretest meal CHO and protein content all affected the BHB response (p<0.001). Conclusion: There was a large inter-individual variability, with phenotype effects identified. This highlights challenges in interpreting clinical responses to MCT intake.

Long-term Physical Exercise Improves Finger Tapping of Patients with Alzheimer's Disease

2021 ◽  
Vol 18 ◽  
Author(s):  
Linlin Zhao ◽  
Guanghua Liu ◽  
Lingli Zhang ◽  
Yuxiang Du ◽  
Le Lei ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Physical Exercise ◽  
Healthy Subjects ◽  
Memory Loss ◽  
Finger Tapping ◽  
Left Hand ◽  
Right Hand ◽  
The Impact

Background: Alzheimer's disease (AD) is a chronic neurodegenerative disease which has been characterized by progressive development of long onset early disease with complicated etiology, and may cause memory loss, cognitive impairment, and behavioral changes. Physical exercise may play a preventive role in AD. In the present study, we investigated the impact of longer-term physical exercise on finger tapping of AD patient by comparing the finger tapping of AD patients and heathy controls without AD. Methods: In this study, 140 subjects who aged ≥ 60 years were enrolled. Group A consisted of 70 subjects (27 males and 43 females) without exercise habits who selected from Yangpu District (Shanghai, China). Group B consisted of 70 subjects (27 males and 43 females) who selected from Minxing District (Shanghai, China). All the subjects were right-handed as well. The subjects’ data, including subjects’ age, weight, height, Montreal Cognitive Assessment (MoCA), Mini-Mental State Examination (MMSE), and finger tapping frequency were measured. Results: The subjects were matched in age, weight, and height. The AD subjects’ MoCA and MMSE scores were noticeably lower than healthy subjects’ scores (P<0.001); besides, AD patients with exercise have significantly lower MoCA and MMSE scores than healthy controls with exercise (P<0.001). The finger tapping of AD subjects’ left hands was significantly lower than that of healthy subjects without AD (P<0.01), and AD subjects with exercise tapped significantly slower with left hand than healthy subjects with exercise (P<0.01). Meanwhile, AD subjects with exercise tapped significantly faster with left hand than AD subjects (P<0.05). The right hands of AD subjects tapped remarkably less than healthy subjects (P<0.01) with or without exercise. Meanwhile, subjects with exercise tapped significantly faster with right hand than healthy subjects (P<0.05), and AD subjects with exercise tapped significantly faster with right hand than AD subjects (P<0.05). Conclusion: Long-term physical exercises can improve finger tapping frequency, especially patients with AD. Finger tapping frequency may be used as an index to monitor cognitive decline in ageing AD patients.

Fluoxetine Protects against Dendritic Spine Loss in Middle-aged APPswe/PSEN1dE9 Double Transgenic Alzheimer’s Disease Mice

2020 ◽  
Vol 17 (1) ◽  
pp. 93-103 ◽  
Author(s):  
Jing Ma ◽  
Yuan Gao ◽  
Wei Tang ◽  
Wei Huang ◽  
Yong Tang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Dendritic Spines ◽  
Dendritic Spine ◽  
Early Stage ◽  
Learning Ability ◽  
Middle Aged ◽  
Protein Levels ◽  
Spine Pathology ◽  
The Impact

Background: Studies have suggested that cognitive impairment in Alzheimer’s disease (AD) is associated with dendritic spine loss, especially in the hippocampus. Fluoxetine (FLX) has been shown to improve cognition in the early stage of AD and to be associated with diminishing synapse degeneration in the hippocampus. However, little is known about whether FLX affects the pathogenesis of AD in the middle-tolate stage and whether its effects are correlated with the amelioration of hippocampal dendritic dysfunction. Previously, it has been observed that FLX improves the spatial learning ability of middleaged APP/PS1 mice. Objective: In the present study, we further characterized the impact of FLX on dendritic spines in the hippocampus of middle-aged APP/PS1 mice. Results: It has been found that the numbers of dendritic spines in dentate gyrus (DG), CA1 and CA2/3 of hippocampus were significantly increased by FLX. Meanwhile, FLX effectively attenuated hyperphosphorylation of tau at Ser396 and elevated protein levels of postsynaptic density 95 (PSD-95) and synapsin-1 (SYN-1) in the hippocampus. Conclusion: These results indicated that the enhanced learning ability observed in FLX-treated middle-aged APP/PS1 mice might be associated with remarkable mitigation of hippocampal dendritic spine pathology by FLX and suggested that FLX might be explored as a new strategy for therapy of AD in the middle-to-late stage.

Emerging Proof of Protein Misfolding and Interactions in Multifactorial Alzheimer's Disease

2020 ◽  
Vol 20 (26) ◽  
pp. 2380-2390 ◽  
Author(s):  
Md. Sahab Uddin ◽  
Abdullah Al Mamun ◽  
Md. Ataur Rahman ◽  
Tapan Behl ◽  
Asma Perveen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Protein Misfolding ◽  
Neurodegenerative Disorder ◽  
Senile Plaques ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Misfolded Proteins ◽  
Cell Organelles ◽  
The Impact

Objective: Alzheimer's disease (AD) is a devastating neurodegenerative disorder, characterized by the extracellular accumulations of amyloid beta (Aβ) as senile plaques and intracellular aggregations of tau in the form of neurofibrillary tangles (NFTs) in specific brain regions. In this review, we focus on the interaction of Aβ and tau with cytosolic proteins and several cell organelles as well as associated neurotoxicity in AD. Summary: Misfolded proteins present in cells accompanied by correctly folded, intermediately folded, as well as unfolded species. Misfolded proteins can be degraded or refolded properly with the aid of chaperone proteins, which are playing a pivotal role in protein folding, trafficking as well as intermediate stabilization in healthy cells. The continuous aggregation of misfolded proteins in the absence of their proper clearance could result in amyloid disease including AD. The neuropathological changes of AD brain include the atypical cellular accumulation of misfolded proteins as well as the loss of neurons and synapses in the cerebral cortex and certain subcortical regions. The mechanism of neurodegeneration in AD that leads to severe neuronal cell death and memory dysfunctions is not completely understood until now. Conclusion: Examining the impact, as well as the consequences of protein misfolding, could help to uncover the molecular etiologies behind the complicated AD pathogenesis.

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