High Levels of Neuroinflammatory Markers driving increased Alzheimer's prevalence among blacks.
Proinflammatory markers appear to be significantly elevated in the brains of black patients with Alzheimer's disease as compared to white patients as reported by the FDA.
Sherry Ferguson, PhD, research psychologist at the FDA National Center for Toxicology Research, said the "brains of black patients studied had significantly higher levels of IL-1beta, TNF-related apoptosis-inducing ligand (TRAIL), and monokine induced by gamma interferon (MIG)."
This proposed pathway may provide an explanation as to why black patients are twice as likely as white patients to develop Alzheimer's.
"The new, unpublished data used this same neuropathological cohort, but examined 40 known neuroinflammatory markers. Compared to the white sample, the black sample showed:
IL-1B, thought to increase amyloid precursor protein and promote tau phosphorylation, increased by 109% MIG, an attractant for activated T-cells, increased by 37% TRAIL, a ligand that induces apoptosis. increased by 50%"
Inflammation causes Alzheimer's. Inflammation from elevated metals, Lyme, infectious agents, chronic food allergies, gluten, medications, toxic stress and more.
Dr. Ferguson postulated that at least some of this neuroinflammatory profile could be related to the formation of inflammasomes – multi-protein oligomeric structures formed in microglia in the brain by the influence of the NLRP3 gene.
“There is a lot of evidence that inflammasomes are involved in AD pathogenesis,” she said. Messenger RNA for the NLRP3 inflammasome is up-regulated in blood from AD patients. Alzheimer’s transgenic mice without the gene show decreased hippocampal and cortical AB40 and 42, increased microglial phagocytosis, and better memory. There is also some evidence that the NLRP3 inflammasome releases minute protein particles called apoptosis-associated (ASC) specks. Some researchers think these particles help seed amyloid throughout the brain. Based on these findings, Dr. Ferguson postulated a potential pathway for the increased prevalence and severity of AD among blacks."
The proinflammatory cytokines are released in a response to rising AB levels, this promotes the formation of the NLRP3 inflammasome. The inflammasome releases more chemokines and cytokines, which then leased to a chronic proinflammatory state and thus leads to synaptic dysfunction, cognitive dysfunction and neuronal death involved in Alzheimer's.
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11, 2. P., & Michele G. Sullivan Clinical Neurology News. (2018, January 16). High levels of neuroinflammatory markers may drive increased Alzheimer's prevalence among blacks. Retrieved January 18, 2018, from https://www.mdedge.com/clinicalneurologynews/article/156099/alzheimers-cognition/high-levels-neuroinflammatory-markers-may?oc_slh=1bfa450258f478dbfd9e69222122108ad78eaa1a91f644b08804e1ea877a5b75&channel=180&utm_source=News_CNN_eNL_011818_HA&utm_medium=email&utm_content=Alzheimer%27s%3A High levels of neuroinflammatory markers among blacks
11, 2. P., & Michele G. Sullivan Clinical Neurology News. (2018, January 16). High levels of neuroinflammatory markers may drive increased Alzheimer's prevalence among blacks. Retrieved January 18, 2018, from https://www.mdedge.com/clinicalneurologynews/article/156099/alzheimers-cognition/high-levels-neuroinflammatory-markers-may?oc_slh=1bfa450258f478dbfd9e69222122108ad78eaa1a91f644b08804e1ea877a5b75&channel=180&utm_source=News_CNN_eNL_011818_HA&utm_medium=email&utm_content=Alzheimer%27s%3A High levels of neuroinflammatory markers among blacks