AI Engines For more Details: Perplexityβ Kagi Labsβ Youβ
Neurological Disorders: Excessive glutamate activity can lead to excitotoxicity, a process where overactivation of glutamate receptors causes neuronal damage or cell death. This is implicated in various neurological disorders such as stroke, traumatic brain injury, epilepsy, Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis (ALS). In these conditions, the excessive release of glutamate and subsequent excitotoxicity contribute to neuronal dysfunction and degeneration.
Migraine: Glutamate has been implicated in the pathophysiology of migraine headaches. Elevated levels of glutamate have been observed in the brains of individuals experiencing migraines, and it is thought to contribute to the initiation and propagation of migraine attacks. Glutamate signaling may also modulate pain pathways involved in migraine headaches.
Neuropsychiatric Disorders: Dysregulation of glutamate neurotransmission has been implicated in various neuropsychiatric disorders, including depression, anxiety disorders, schizophrenia, and obsessive-compulsive disorder (OCD). Glutamate receptors and synaptic plasticity mechanisms involving glutamate signaling are believed to play a role in the pathophysiology of these conditions.
Neurodevelopmental Disorders: Altered glutamate signaling during critical periods of brain development has been associated with neurodevelopmental disorders such as autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD). Dysregulation of glutamate receptors and synaptic function may contribute to the cognitive and behavioral impairments observed in these conditions.
Glutamate Excitotoxicity in Ischemic Stroke: In ischemic stroke, reduced blood flow to the brain leads to decreased oxygen and glucose supply, resulting in neuronal injury and cell death. Glutamate excitotoxicity exacerbates neuronal damage during ischemic stroke, as excessive glutamate release overactivates glutamate receptors, leading to calcium influx, oxidative stress, and neuronal death.
Degenerative Disorders: Glutamate excitotoxicity has also been implicated in the pathogenesis of degenerative disorders affecting the retina and inner ear. In conditions such as age-related macular degeneration (AMD) and certain forms of sensorineural hearing loss, excessive glutamate release and excitotoxicity contribute to neuronal degeneration and functional impairment.
Metabolic Syndrome: Emerging research suggests a potential link between glutamate signaling and metabolic disorders such as obesity and type 2 diabetes. Glutamate receptors are expressed in peripheral tissues involved in energy metabolism, and alterations in glutamate signaling may influence metabolic homeostasis and contribute to insulin resistance and obesity-related complications.
We extend modifiers to include items that changes the parent and child taxa. I.e. for a species, that would be the genus that is belongs to and the strains in the species.
A higher number indicates impact on more bacteria associated with the condition and confidence on the impact.
We have X bacteria high and Y low reported. We find that the modifier reduces some and increases other of these two groups. We just tally: X|reduces + Y|Increase = Positive β X|increases + Y|decrease = Negative.
Benefit Ratio:
Numbers above 0 have increasing positive effect.
Numbers below 0 have increasing negative effect.