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Neuroplasticity is the process by which neurons adapt to a disturbance over time, and most often occurs in response to repeated exposure to stimuli. [27] Aerobic exercise increases the production of neurotrophic factors [note 1] (e.g., BDNF, IGF-1, VEGF) which mediate improvements in cognitive functions and various forms of memory by promoting blood vessel formation in the brain, adult ...
Brain death is used as an indicator of legal death in many jurisdictions, [7] but it is defined inconsistently and often confused by the public. [8] Various parts of the brain may keep functioning when others do not anymore, and the term "brain death" has been used to refer to various combinations.
The phenomenon has been observed to occur several minutes after the removal of medical ventilators used to pump air in and out of brain-dead patients. [4] It also occurs during testing for apnea—that is, suspension of external breathing and motion of the lung muscles—which is one of the criteria for determining brain death used for example by the American Academy of Neurology.
Subtle changes in brain activity in the presence of both amyloid-beta and tau proteins may point to Alzheimer's disease, long before symptoms appear, a new study indicates.
Traumatic brain injury is defined as damage to the brain resulting from external mechanical force, such as rapid acceleration or deceleration, impact, blast waves, or penetration by a projectile. [10] Brain function is temporarily or permanently impaired and structural damage may or may not be detectable with current technology. [11]
Other symptoms include difficulty speaking, slurred speech, and the loss of coordination. [8] The symptoms of brain ischemia range from mild to severe. Further, symptoms can last from a few seconds to a few minutes or extended periods of time. If the brain becomes damaged irreversibly and infarction occurs, the symptoms may be permanent. [9]
Aβ was found manipulating the level of nicotine in the brain along with the MAP kinase, another signaling receptor, to cause cell death. Another chemical in the brain that Aβ regulates is JNK; this chemical halts the extracellular signal-regulated kinases (ERK) pathway, which normally functions as memory control in the brain. As a result ...
In other areas of the brain, viable human neurons have been recovered and grown in culture hours after clinical death. [10] Brain failure after clinical death is now known to be due to a complex series of processes called reperfusion injury that occur after blood circulation has been restored, especially processes that interfere with blood ...