Search results
Results from the WOW.Com Content Network
The brain is more vulnerable to oxidative stress than other organs, due to its low oxidative capacity. Because neurons are characterized as postmitotic cells, meaning that they live with accumulated damage over the years, accumulation of ROS is fatal. Thus, increased levels of ROS age neurons, which leads to accelerated neurodegenerative ...
The SCA1 mice experience increased oxidative stress and increased oxidative DNA damage. [90] The mitochondrial targeted antioxidant MitoQ was found to slow down the appearance of SCA1-linked neuropathologies such as lack of motor coordination. MitoQ also prevented oxidative stress induced DNA damage and Purkinje cell loss. [90]
Brain trauma or stroke can cause ischemia, in which blood flow is reduced to inadequate levels. Ischemia is followed by accumulation of glutamate and aspartate in the extracellular fluid , causing cell death, which is aggravated by lack of oxygen and glucose .
Stress can cause acute and chronic changes in certain brain areas which can cause long-term damage. [4] Over-secretion of stress hormones most frequently impairs long-term delayed recall memory, but can enhance short-term, immediate recall memory. This enhancement is particularly relative in emotional memory.
The activation of the facial motor nucleus causes a jerk of the head while an activation in the spinal cord causes the whole body to startle. [ 6 ] During neuromotor examinations of newborns, it is noted that, for a number of techniques, the patterns of the startle reaction and the Moro reflex may significantly overlap, the notable distinction ...
There exist studies on germ-free mice, devoid of any gut bacteria, that show the mice exhibit less anxiety compared to mice with a normal gut microbiome. [ 40 ] [ 41 ] Inflammations or infections of the gut tract of mice caused a change in certain behaviour associated with symptoms of anxiety, such as a less drive to explore [ 42 ] and a ...
In many protocols, mice are coinjected with pertussis toxin to break down the blood-brain barrier and allow immune cells access to the CNS tissue. This immunisation leads to multiple small disseminated lesions of demyelination (as well as micro-necroses) in the brain and spinal cord and the onset of clinical symptoms. [citation needed]
Neuronal activity at the microscopic level has a stochastic character, with atomic collisions and agitation, that may be termed "noise." [4] While it isn't clear on what theoretical basis neuronal responses involved in perceptual processes can be segregated into a "neuronal noise" versus a "signal" component, and how such a proposed dichotomy could be corroborated empirically, a number of ...