Neuroinflammation and what it means in AUTISM and PANS/PANDAS

Neuroinflammation, which refers to inflammation within the brain and spinal cord, has been increasingly recognized as a significant factor in the development and

manifestation of autistic symptoms. When a sudden flair of symptoms or regression occurs, understanding the processes that may be contributing to increased neurological inflammation may be the key to successfully treating the flair, addressing regression, and decreasing the manifestation of autistic symptoms. In practice, we want to identify if the patient has increased or unmanageable systemic inflammation and understand what may be triggering or driving this, factors can be metabolic and immunological, pathogenic, toxic, nutrient driven and even trauma activated.

Here's how neuroinflammation can contribute to the various symptoms seen in autism spectrum disorder (ASD):

Mechanisms of Neuroinflammation in Autism

1. Immune System Dysregulation:

Microglial Activation: Microglia are the primary immune cells in the brain. In ASD,

microglia can become chronically activated, releasing pro-inflammatory cytokines

and other inflammatory mediators.

Cytokine Imbalance:

Elevated levels of pro-inflammatory cytokines ( e.g., IL-6, TNF-α) and reduced levels

of anti-inflammatory cytokines can create a persistent inflammatory state in the

brain. IL-6 incidentally is strongly linked to neuroinflammation and levels are increased in cases of Lyme Disease and mercury toxicity in the system.

2. Blood-Brain Barrier (BBB) Disruption:

Increased Permeability:

Chronic inflammation can compromise the integrity of the BBB, allowing immune

cells and inflammatory molecules to enter the brain from the periphery.

Immune Cell Infiltration:

This disruption can lead to the infiltration of peripheral immune cells into the brain,

exacerbating neuroinflammation.

3. Oxidative Stress:

Reactive Oxygen Species (ROS):

Inflammatory processes can increase the production of ROS, leading to oxidative

stress, which damages neurons and other brain cells.

Antioxidant Defenses:

Neuroinflammation can overwhelm the brain's antioxidant defenses, further

contributing to cellular damage.

Impact on Brain Function and Development

1. Synaptic Dysfunction:

Synaptic Pruning:

Microglia play a role in synaptic pruning during brain development. Chronic

activation of microglia can lead to excessive or insufficient pruning, affecting

neural connectivity and function.

Neurotransmitter Imbalance:

Inflammatory cytokines can alter the synthesis, release, and reuptake of

neurotransmitters such as serotonin, dopamine, and glutamate, leading to

imbalances that affect behavior and cognition

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2. Neurogenesis and Neuronal Survival:

Inhibited Neurogenesis:

Chronic inflammation can inhibit neurogenesis (the formation of new neurons)

and promote apoptosis (cell death), which can disrupt normal brain development.

Neuron Viability:

Pro-inflammatory cytokines can be neurotoxic, leading to neuron damage or

death, which can affect brain regions involved in social behavior, communication,

and executive function.

3. Glial Cell Dysfunction:

Astrocytes:

Inflammation can impair the function of astrocytes, which are critical for

maintaining the extracellular environment, providing metabolic support to

neurons, and modulating synaptic transmission.

Oligodendrocytes:

Inflammation can also affect oligodendrocytes, which are responsible for

myelinating axons. This can lead to disruptions in the speed and efficiency of

neural signaling.

Manifestation of Autistic Symptoms

1. Social Communication Deficits:

Neural Connectivity:

Altered synaptic pruning and neurotransmitter imbalances can affect neural

circuits involved in social behavior and communication.

Social Processing:

Inflammation in regions like the prefrontal cortex and amygdala can impair social

processing, leading to difficulties in understanding social cues and engaging in

social interactions.

2. Repetitive Behaviors and Restricted Interests:

Basal Ganglia Dysfunction:

Inflammation in the basal ganglia, a region involved in motor control and habit

formation, can contribute to repetitive behaviors and restricted interests.

Cortical Networks:

Disruptions in cortical networks due to neuroinflammation can affect cognitive

flexibility, leading to rigid thinking and repetitive patterns of behavior.

3. Sensory Processing Issues:

Sensory Cortices:

Neuroinflammation in sensory cortices can lead to altered sensory processing,

contributing to hypersensitivity or hyposensitivity to sensory stimuli.

Integration: Inflammation can affect the integration of sensory information, leading to

difficulties in processing and responding appropriately to sensory inputs.

4. Cognitive and Behavioral Challenges:

Executive Function:

Inflammation in the prefrontal cortex can impair executive functions such as planning,

decision-making, and impulse control.

Learning and Memory:

Hippocampal inflammation can affect learning and memory

processes, leading to difficulties in acquiring and retaining new information.

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