scholarly journals Cordyceps cicadae NTTU 868 Mycelium with The Addition of Bioavailable Forms of Magnesium from Deep Ocean Water Prevents the Aβ40 and Streptozotocin-Induced Memory Deficit via Suppressing Alzheimer’s Disease Risk Factors and Increasing Magnesium Uptake of Brain

Fermentation ◽  
2021 ◽  
Vol 7 (1) ◽  
pp. 39
Author(s):  
Yan-Zhong Wu ◽  
Chun-Lin Lee

Alzheimer’s disease (AD) is a common neurodegenerative disease characterized by continuous accumulation of β-amyloid (Aβ) in the brain. Deep ocean water (DOW) with rich inorganic salts and minerals was proven to promote fungi growth and metabolism. Cordyceps cicada, a functional food fungus, can produce higher anti-oxidant and anti-inflammatory compounds including adenosine, polysaccharide, and N(6)-(2-Hydroxyethyl) adenosine (HEA). This study used DOW as the culture water of C. cicadae NTTU 868 for producing DOW-cultured C. cicadae (DCC), and further investigated the effects and mechanisms on improving the memory deficit and repressing risk factors expressions in Aβ40 and streptozotocin (STZ)-induced Alzheimer’s disease rats model. In the results, DCC including mycelium and filtrate had adenosine, HEA, polysaccharide, and intracellular Mg2+ after fermentation with DOW. DCC had more effect on the improvement of memory deficit because it suppressed Aβ40 and streptozotocin (STZ) infusion caused BACE, pro-inflammatory factors expressions, and Aβ40 accumulation by increasing sRAGE expression in the brain. Furthermore, DCC enhanced the MAGT1 expression due to high organic magnesium, which can reverse Aβ40-induced cortex magnesium deficiency and further repress Aβ40 accumulation.

2020 ◽  
Vol 21 (21) ◽  
pp. 8338
Author(s):  
Kimberley D. Bruce ◽  
Maoping Tang ◽  
Philip Reigan ◽  
Robert H. Eckel

Lipoprotein lipase (LPL) is a key enzyme in lipid and lipoprotein metabolism. The canonical role of LPL involves the hydrolysis of triglyceride-rich lipoproteins for the provision of FFAs to metabolic tissues. However, LPL may also contribute to lipoprotein uptake by acting as a molecular bridge between lipoproteins and cell surface receptors. Recent studies have shown that LPL is abundantly expressed in the brain and predominantly expressed in the macrophages and microglia of the human and murine brain. Moreover, recent findings suggest that LPL plays a direct role in microglial function, metabolism, and phagocytosis of extracellular factors such as amyloid- beta (Aβ). Although the precise function of LPL in the brain remains to be determined, several studies have implicated LPL variants in Alzheimer’s disease (AD) risk. For example, while mutations shown to have a deleterious effect on LPL function and expression (e.g., N291S, HindIII, and PvuII) have been associated with increased AD risk, a mutation associated with increased bridging function (S447X) may be protective against AD. Recent studies have also shown that genetic variants in endogenous LPL activators (ApoC-II) and inhibitors (ApoC-III) can increase and decrease AD risk, respectively, consistent with the notion that LPL may play a protective role in AD pathogenesis. Here, we review recent advances in our understanding of LPL structure and function, which largely point to a protective role of functional LPL in AD neuropathogenesis.


2018 ◽  
Vol 9 ◽  
Author(s):  
Atsuko Katsumoto ◽  
Hideyuki Takeuchi ◽  
Keita Takahashi ◽  
Fumiaki Tanaka

2019 ◽  
Vol 7 (26) ◽  
pp. 4124-4132 ◽  
Author(s):  
Siyue Ma ◽  
Jiabao Qiang ◽  
Linyang Li ◽  
Yan Mo ◽  
Mengyao She ◽  
...  

An efficient biosensor to monitor Alzheimer's disease risk factors and inhibit Alzheimer's disease by disaggregating Aβ aggregation.


2012 ◽  
Vol 15 (3) ◽  
pp. 286-295 ◽  
Author(s):  
Derrek P. Hibar ◽  
Neda Jahanshad ◽  
Jason L. Stein ◽  
Omid Kohannim ◽  
Arthur W. Toga ◽  
...  

The development of late-onset Alzheimer's disease (LOAD) is under strong genetic control and there is great interest in the genetic variants that confer increased risk. The Alzheimer's disease risk gene, growth factor receptor bound protein 2-associated protein (GAB2), has been shown to provide a 1.27–1.51 increased odds of developing LOAD for rs7101429 major allele carriers, in case-control analysis. GAB2 is expressed across the brain throughout life, and its role in LOAD pathology is well understood. Recent studies have begun to examine the effect of genetic variation in the GAB2 gene on differences in the brain. However, the effect of GAB2 on the young adult brain has yet to be considered. Here we found a significant association between the GAB2 gene and morphological brain differences in 755 young adult twins (469 females) (M = 23.1, SD = 3.1 years), using a gene-based test with principal components regression (PCReg). Detectable differences in brain morphology are therefore associated with variation in the GAB2 gene, even in young adults, long before the typical age of onset of Alzheimer's disease.


2005 ◽  
Vol 18 (2) ◽  
pp. 335-340 ◽  
Author(s):  
Jerson Laks ◽  
Roberto Miotto ◽  
Valeska Marinho ◽  
Eliasz Engelhardt

We report the case of an elderly woman with Alzheimer's disease, risk factors for vascular dementia, and atrium-ventricular blockade, who presented with severe agitation and psychosis. She was treated with aripiprazole and assessed with the Neuropsychiatric Inventory (NPI) over the course of 14 weeks. NPI scores showed a marked decrease in psychosis and agitation at week 4, and complete recovery at week 14, except for depression.


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