Diminished brain resilience syndrome: A modern day neurological pathology of increased susceptibility to mild brain trauma, concussion, and downstream neurodegeneration

Morley, Wendy A.; Seneff, Stephanie

doi:10.4103/2152-7806.134731

Cited by 14 publications

(16 citation statements)

References 206 publications

(282 reference statements)

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“…The few studies utilizing DTI to investigate the chronic effects of head trauma >2 years post-injury report significantly impaired WM integrity that correlates with cognitive impairment (Kraus et al, 2007 ; Geary et al, 2010 ; Little et al, 2010 ). It is plausible that much of the damage done to the axons occurs secondarily to the initial injury through complex biological mechanisms that may not be observable in the early phases of recovery (Morley and Seneff, 2014 ). It is important for future studies to observe those with frequent exposure to head trauma longitudinally, even after exposure to head trauma has ended.…”

Section: Discussion and Future Directionsmentioning

confidence: 99%

“…It is still unclear how other factors like gender, age at youngest head injury, and education may influence risk of developing this disease. Other environmental risk factors include exposure to neurotoxins like glyphophosate, which are found in herbicides, and addiction to methamphetamines (Sekine et al, 2008 ; Morley and Seneff, 2014 ). There may also be an inherent risk for CTE that is determined by genetic make-up.…”

Section: Chronic Traumatic Encephalopathymentioning

confidence: 99%

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Neuroimaging assessment of early and late neurobiological sequelae of traumatic brain injury: implications for CTE

2015

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Traumatic brain injury (TBI) has been increasingly accepted as a major external risk factor for neurodegenerative morbidity and mortality. Recent evidence indicates that the resultant chronic neurobiological sequelae following head trauma may, at least in part, contribute to a pathologically distinct disease known as Chronic Traumatic Encephalopathy (CTE). The clinical manifestation of CTE is variable, but the symptoms of this progressive disease include impaired memory and cognition, affective disorders (i.e., impulsivity, aggression, depression, suicidality, etc.), and diminished motor control. Notably, mounting evidence suggests that the pathology contributing to CTE may be caused by repetitive exposure to subconcussive hits to the head, even in those with no history of a clinically evident head injury. Given the millions of athletes and military personnel with potential exposure to repetitive subconcussive insults and TBI, CTE represents an important public health issue. However, the incidence rates and pathological mechanisms are still largely unknown, primarily due to the fact that there is no in vivo diagnostic tool. The primary objective of this manuscript is to address this limitation and discuss potential neuroimaging modalities that may be capable of diagnosing CTE in vivo through the detection of tau and other known pathological features. Additionally, we will discuss the challenges of TBI research, outline the known pathology of CTE (with an emphasis on Tau), review current neuroimaging modalities to assess the potential routes for in vivo diagnosis, and discuss the future directions of CTE research.

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Section: Discussion and Future Directionsmentioning

confidence: 99%

Section: Chronic Traumatic Encephalopathymentioning

confidence: 99%

Neuroimaging assessment of early and late neurobiological sequelae of traumatic brain injury: implications for CTE

2015

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“…This indiscriminate efflux of glutamate followed by an influx of Ca++ is a critical step in glutamate excitotoxicity, which is central to secondary axonal injury. This is a delayed degenerative process that involves, among other things, lethal metabolic changes, free radical generation, and mitochondrial dysfunction, which ultimately leads to axonal disconnection and neuronal death ( 8 , 9 , 15 ).…”

Section: Neuroimmune Activation Ionic Shifts and Cellular Fluxmentioning

confidence: 99%

“…This review article explores two novel concepts: environmental subconcussive injury (ESCI), a term coined by the author to depict environmental toxicant exposure sufficient to stimulate neuroimmune activation, ionic shifts, and other secondary neurochemical events resulting in axonal injury, and diminished brain resilience (DBR), a concept first presented by the author in 2014 to describe a specific physiological state of nutritional functional deficiencies and altered microbiome created by modern-day exposures and lifestyle choices that lead to a diminished capacity to respond and recover from brain insults ( 15 ).…”

Section: Introductionmentioning

confidence: 99%

Environmental Subconcussive Injury, Axonal Injury, and Chronic Traumatic Encephalopathy

Morley¹

2018

Front. Neurol.

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Brain injury occurs in two phases: the initial injury itself and a secondary cascade of precise immune-based neurochemical events. The secondary phase is typically functional in nature and characterized by delayed axonal injury with more axonal disconnections occurring than in the initial phase. Axonal injury occurs across the spectrum of disease severity, with subconcussive injury, especially when repetitive, now considered capable of producing significant neurological damage consistent with axonal injury seen in clinically evident concussion, despite no observable symptoms. This review is the first to introduce the concept of environmental subconcussive injury (ESCI) and sets out how secondary brain damage from ESCI once past the juncture of microglial activation appears to follow the same neuron-damaging pathway as secondary brain damage from conventional brain injury. The immune response associated with ESCI is strikingly similar to that mounted after conventional concussion. Specifically, microglial activation is followed closely by glutamate and calcium flux, excitotoxicity, reactive oxygen species and reactive nitrogen species (RNS) generation, lipid peroxidation, and mitochondrial dysfunction and energy crisis. ESCI damage also occurs in two phases, with the primary damage coming from microbiome injury (due to microbiome-altering events) and secondary damage (axonal injury) from progressive secondary neurochemical events. The concept of ESCI and the underlying mechanisms have profound implications for the understanding of chronic traumatic encephalopathy (CTE) etiology because it has previously been suggested that repetitive axonal injury may be the primary CTE pathogenesis in susceptible individuals and it is best correlated with lifetime brain trauma load. Taken together, it appears that susceptibility to brain injury and downstream neurodegenerative diseases, such as CTE, can be conceptualized as a continuum of brain resilience. At one end is optimal resilience, capable of launching effective responses to injury with spontaneous recovery, and at the other end is diminished resilience with a compromised ability to respond and/or heal appropriately. Modulating factors such as one’s total cumulative and synergistic brain trauma load, bioavailability of key nutrients needed for proper functioning of restorative metabolic pathways (specifically those involved in the deactivation and clearance of metabolic by-products of brain injury) are key to ultimately determining one’s brain resilience.

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“…Glyphosate also chelates aluminum,[ 230 ] and it has been reasoned that this enables aluminum to get past the gut barrier more readily through direct analogy with the situation with arsenic, which is also a 3+ cation. [ 193 ]…”

Section: Analogy With Arsenic and Aluminummentioning

confidence: 99%

Glyphosate, pathways to modern diseases III: Manganese, neurological diseases, and associated pathologies

Samsel

Seneff²

2015

Surg Neurol Int

Self Cite

113

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Manganese (Mn) is an often overlooked but important nutrient, required in small amounts for multiple essential functions in the body. A recent study on cows fed genetically modified Roundup®-Ready feed revealed a severe depletion of serum Mn. Glyphosate, the active ingredient in Roundup®, has also been shown to severely deplete Mn levels in plants. Here, we investigate the impact of Mn on physiology, and its association with gut dysbiosis as well as neuropathologies such as autism, Alzheimer's disease (AD), depression, anxiety syndrome, Parkinson's disease (PD), and prion diseases. Glutamate overexpression in the brain in association with autism, AD, and other neurological diseases can be explained by Mn deficiency. Mn superoxide dismutase protects mitochondria from oxidative damage, and mitochondrial dysfunction is a key feature of autism and Alzheimer’s. Chondroitin sulfate synthesis depends on Mn, and its deficiency leads to osteoporosis and osteomalacia. Lactobacillus, depleted in autism, depend critically on Mn for antioxidant protection. Lactobacillus probiotics can treat anxiety, which is a comorbidity of autism and chronic fatigue syndrome. Reduced gut Lactobacillus leads to overgrowth of the pathogen, Salmonella, which is resistant to glyphosate toxicity, and Mn plays a role here as well. Sperm motility depends on Mn, and this may partially explain increased rates of infertility and birth defects. We further reason that, under conditions of adequate Mn in the diet, glyphosate, through its disruption of bile acid homeostasis, ironically promotes toxic accumulation of Mn in the brainstem, leading to conditions such as PD and prion diseases.

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Diminished brain resilience syndrome: A modern day neurological pathology of increased susceptibility to mild brain trauma, concussion, and downstream neurodegeneration

Cited by 14 publications

References 206 publications

Neuroimaging assessment of early and late neurobiological sequelae of traumatic brain injury: implications for CTE

Neuroimaging assessment of early and late neurobiological sequelae of traumatic brain injury: implications for CTE

Environmental Subconcussive Injury, Axonal Injury, and Chronic Traumatic Encephalopathy

Glyphosate, pathways to modern diseases III: Manganese, neurological diseases, and associated pathologies

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