What is Neuroinflammation?
Neuroinflammation is an inflammatory response within the brain. Neuroinflammation is a localized inflammation in the peripheral nervous system (PNS) and central nervous system (CNS). This type of inflammation is triggered by nerve activation and has many harmful side effects. It’s important to take brain inflammation seriously because it can rapidly increase the risk of dementia, Alzheimer’s, Parkinson’s, and other brain degenerative diseases.
Factors that cause Neuroinflammation
Diabetes and high blood sugar
Poor circulation, lack of exercise, chronic stress, heart failure, respiratory issues, anemia
Previous head trauma
Neurological autoimmunity
Eating gluten when you are gluten intolerant
Poor brain antioxidant status
Alcohol and drug abuse
Environmental pollutants
Systemic inflammation
Inflammatory bowel conditions
Leaky blood-brain barrier
Do you think you have Neuroinflammation?
Here are some symptoms:
Brain fog
Unclear thoughts
Low brain endurance
Slow and varied mental speeds
Loss of brain function after trauma
Brain fatigue and poor mental focus after meals
Brain fatigue promoted by systemic inflammation
Brain fatigue promoted by chemicals, scents, and pollutants
How does Neuroinflammation work?
At the root of brain inflammation are microglia cells, the brain’s immune cells. They were once considered simply to be glue that held neurons together, but newer research shows how important to brain function they are. In fact, they outnumber neurons ten to one. When the brain is healthy the microglia dispose of dead neurons, beta amyloid plaque, and other debris that interfere with healthy communication between neurons. They also facilitate healthy neuron metabolism and neuron synapses (Schmoe 1).
However, when something triggers inflammation in the brain, the glia cells switch into attack mode. This hinders communication between neurons so they fire more slowly, creating symptoms such as brain fog, slower mental speed, slower recall, and slower reflexes. Brain inflammation also shuts down energy production in the neurons, so brain endurance drops, making it harder to read, work, or concentrate for any length of time. (Schmoe 1).
Neuroinflammation Linked to Depression?!
One of the most common mental disorders, major depressive disorder (MDD) has been shown to significantly increase the risk of harmful medical conditions for individuals, such as death. People that have MDD have shown levels of translocator protein (TSPO), a marker of microglial inflammation, which have increased, new research shows.
“The evidence for a link between depression and neuroinflammation is quite compelling now, and there is also mounting evidence for a link between suicide and inflammation across a range of mental disorders,” lead investigator Peter S. Talbot, MD.
“If we can learn more about these links, it may lead to more effective prevention or treatments of depression and suicidal thinking by targeting specific aspects of the inflammatory process,” he added. Inflammation in depression is a “promising avenue of research for new treatment strategies, based on evidence that at least a subset of individuals with MDD have higher levels of peripheral proinflammatory cytokines,” the authors wrote.
Evidence of an association between neuroinflammation ― specifically, microglial activation ― and suicidality has been based on postmortem studies. No previous research has specifically investigated the association between neuroinflammation and suicidality in living patients. Positron-emission tomography (PET) scans and radioligands specific for the 18-kDa TSPO, a mitochondrial protein that is upregulated in activated glial cells, provide a useful index for measuring neuroinflammation in living patients (Rossa 1).
The researchers set out “to investigate brain TSPO availability in MDD and to explore factors that might be associated with heightened inflammation” using the “prototypical” TSPO radioligand [11C] (R )-PK11195 to measure brain TSPO availability in nonsmoking, medically healthy, and antidepressant-naive or antidepressant-free patients with moderate to severe depression. Three areas of the brain were chosen as the focus of the study: the ACC, the prefrontal cortex (PFC), and the insula. These areas were chosen because in a previous study, TSPO levels in these areas were to be significantly elevated in patients with depression. These areas also play a role in mood regulation, and previous research has found that the ACC (anterior cingulate cortex) has a role in the association between inflammation and depression (Rossa 1).
Commenting on the study for Medscape Medical News, Jonathan P. Godbout, PhD, professor in the Neuroscience Institute for Behavioral Medicine Research, Ohio State Wexner Medical Center, Columbus, described the study as “a good starting point to say neuroinflammation in depression is real and is a target for intervention” because “we need ways to determine neuroinflammation in living, breathing human beings instead of relying on postmortem studies.”
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