Lundgaard Et Al. (2015) Also Recognized The Conflicting

Biologically, sugar effects the brain very dramatically than what they knew around the 1700- 1900’s. When sugar is in your bloodstream the body reacts the same way as if

In the Summer of 2015 I had the opportunity of accomplishing my own research project. With the help of my graduate student, I led us to better understand the neural pathway

Similarly, an increase in the levels of lipid peroxidation was observed in Aβ-induced rat hippocampal cells, confirming previous reports [17]. Enzymatic antioxidants such as SOD, catalase, and GPX act as the cellular antioxidant defense mechanism against free radicals. Since NADPH is required for the regeneration of catalase from its inactive form, catalase activity might be decreased in Aβ induced toxicity due to reduced NADPH levels. In this study, we have reported that Honokiol treatment significantly increased the enzymatic antioxidant activities in APP-CHO cells. In addition, non-enzymatic antioxidants like GSH also exhibited beneficial neuroprotective effects against oxidative stress. GSH is an endogenous nonenzymatic antioxidant that prevents damage to cellular components caused by ROS such as free radicals and peroxides. GSH is oxidized to glutathione disulfide (GSSG) by ROS, thereby causing a reduction in the level of GSH. GR reduces GSSG to GSH via NADPH, which in turn is released by glucose-6-phosphate dehydrogenase [18]. Honokiol treatment upregulated the activity of these antioxidants in APP-CHO cells. In addition to oxidative stress, a strong association between insulin resistance and the development of AD has been demonstrated. Several studies have reported that insulin resistance (IR), an underlying characteristic of type 2 diabetes, is an important risk factor for AD

“Without Hex-A, a fatty substance, or lipid, called GM2 ganglioside accumulates abnormally in cells, especially in the nerve cells of the brain. This ongoing accumulation causes progressive damage to the cells.”http://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0024672/

A cohort of mice underwent a second mTBI after 24 hours. Mice from both WT and Tg groups were assessed 2 days, 9 weeks, and 16 weeks after mTBI treatment. Primarily, H&E stain was employed along with Gomori’s iron stain to localize site and severity of mTBI injury. The degree of A deposition in the somatosensory cortex (SSC), the perihippocampal cortex (PHC), and the hippocampus (HP) of both hemispheres was determined by 4G8 immunostaining. In addition, GFAP staining was used to quantify the population of astrocytes at the site of the injury. Furthermore, Sandwich ELISA was utilized in mice groups 16 weeks after injury to measure A40 and A42 peptide levels in various brain regions, including the cerebral cortex, the hippocampus, and the cerebellum. Such tissues were also analyzed for isoprostane levels that are produced by lipid peroxidation. Isoprostanes were also detected in urine samples at various survival periods. Moreover, mice underwent Morison water maze (MWM) and composite neuroscore (NS) tests at 16 weeks’ post-injury to examine cognitive and motor functions respectively. Uryu and collegues found a significant increase in iron deposits and reactive astrocytes in the repetitive mTBI postmortem sections of Tg mice, when compared to other groups at 16 weeks after the injury. This was not the case in WT mice. Similarly, there was a significant increase in the A burden within select brain regions (i.e. SSC, PHC, HP) of single and

It is a well-known biomarker of brain injury associated with Alzheimer’s disease, concussion and epilepsy. Based on literature review, an overproduction of soluble S100B from the astrocytes binds to the receptor for advanced glycation end products (RAGE) leading to various responses including increased reactive oxygen species (ROS) formation, release of pro-inflammatory markers, and activation of stress response kinases resulting in neuronal cell death. The ongoing neuronal injury and inflammation further promotes cellular apoptosis and impairs neurogenesis in epileptic brain. Identification of this mechanistic relationship between acquired epilepsy and inflammation will provide an important therapeutic target pathway for prevention of

Because of the lack of β-hexosaminidase A, the body cannot break down excess GM2 ganglioside and the fatty substance is able to build up profusely in the nerves and tissues of the brain.

Two varieties of modest terminals were surgically embedded into his somatosensory cortex. Utilizing the clusters, the analysts empowered neurons in the locale with little heartbeats of power. The member announced feeling diverse characteristic sensations -, for example, crushing, tapping, a feeling of upward movement, and a few others - that would fluctuate in sort, power, and area relying upon the recurrence, plentifulness, and area of incitement from the exhibits. It is the first run through such common sensations have been incited by intracortical neural

Sensory organs are metabolically expensive both during development and daily use. Neural tissues including sensory receptor cells require high ATP consumption and neuronal ganglia and the costs are equally high at rest. An investment in a large organ is an indirect indication of its functional importance. A large size of a sensory organ indicates

Astrocytes have been shown to communicate amongst themselves, as well as participate in bidirectional communication with neurons via the 'Tripartite synapse '. Ca2+-dependent glutamate release also

I have elected to pursue research in the field of neuroscience because I relish the approach of logical thinking to satisfy the curiosity of knowing things about me and the world around me. Neuroscience is a fascinating area with a limitless possibility of understanding and uncovering to resolve so many unanswered and unimagined questions. Although, in recent years, a large number of breakthroughs research have been done in the area of neuroscience, still, there is a lot more to discover and untangle in this area. Such an enormous amount of research work in this area has led open to the advancement in the diagnosis and therapeutic approaches to several neurological disorders and cancer such as glioma. Therefore, I decided

Primary cortical mixed neuron-astroglia cultures were prepared from embryonic day 18 Sprague–Dawley rat fetuses and plated on poly-L-lysine coated 12-well plates (Erie Scientific, Portsmouth, NH, USA). Cells were allowed to grow in an atmosphere of 10% CO2 at 37°C for 3 days and then treated with 1 mM 4-amino-6-hydrazino-7-D-ribofuranosyl-7H-pyrrolo (2,3-D)-pyrimidine-5-carboxamide (ARC) for 2 days. The ARC was removed, and fresh 10% plasma-derived horse serum (PDHS) in DMEM was added, after which the cells were grown for an additional 10 to 14 days in 12-well plates {Yang:2014cx}. For cytotoxic challenges, in addition to untreated controls, the following conditions were used: calcium ionophore A23187 (25 μM; Sigma, St Louis, MO, USA) as a

Human brain consists of billions of cells interconnected together, with each performing its separate functions. It consists of two explicit categories of nerves: neurons and glia cells. Neuron is a single nerve cell in the entire nervous system; which is electrically excitable cell that carries information after being processed via chemical or electrical signals. One of its key characteristics is that it does not undergo cell division. In addition, it maintains a voltage gradient for all the neurons across its membranes. Glia cells, on the other hand, its functionality is to maintain homeostasis.

Because virtually no glucose is stored in the brain, the supply of glucose also must be continuous. If the blood entering the brain has a low level of glucose, mental confusion, dizziness, convulsions, and loss of consciousness may occur.

Glucose – why we need it and why it shouldn’t get too high or too low