Dr. Alex Jimenez, El Paso's Chiropractor
I hope you have enjoyed our blog posts on various health, nutritional and injury related topics. Please don't hesitate in calling us or myself if you have questions when the need to seek care arises. Call the office or myself. Office 915-850-0900 - Cell 915-540-8444 Great Regards. Dr. J

Functional Neurology: Glutamate Dysregulation and Excitotoxicity

Excitotoxicity is characterized as an acute insult which causes nerve cell death due to the excessive activation of iGluRs. Acute excitotoxicity plays a fundamental role in a variety of central nervous system (CNS) health issues, including cerebral ischemia, TBI, and status epilepticus. The mechanisms for acute excitotoxicity are different for every health issue.  


With brain ischemia, L-glutamate-associated and L-aspartate-associated excitotoxicity happen within minutes due to the growth in extracellular cerebral L-glutamate as well as L-aspartate. Because these are also energy-dependent, the abrupt loss of energy due to the shut down of blood flow can ultimately breakdown the neuronal and astroglial membrane. In neurons, membrane depolarization contributes to vesicular discharge. Additionally, energy degradation may even cause a change in their action, therefore, causing L-glutamate and L-aspartate to activate and affect ionic homeostasis which can interrupt EAAT action. The activation of L-glutamate/L-aspartate contributes to excitotoxicity through the over-activation of iGluRs of the NMDA type as demonstrated by the efficiency of NMDA antagonists in animal models of transient cerebral ischemia.  


In TBI, the mechanical tissue damage and the disruption of the blood-brain barrier can trigger acute secondary neurodegeneration, which, together with neuroinflammation and oxidative stress, is associated with L-glutamate activation from intracellular compartments and, therefore, by acute excitotoxicity. Moveover, acute application of the NMDA antagonist MK801 following TBI ameliorates neuronal loss and long-term behavioral abnormalities, among others.  


In status epilepticus, continuing the synchronized activity of excitatory neuronal networks as well as the continuous breakdown of restricting mechanisms is the main source of L-glutamate and L-aspartate activation. As the severity of synchronous activity depends upon the involvement of nerve cells into a neuronal system as well as the capability of a neural cell to withstand excess glutamate mainly depends on the expression pattern of iGluRs, a somewhat restricted and maturation-associated degeneration of neuronal populations which is ultimately caused by prolonged epileptic seizures. The significance of excitotoxicity in status epilepticus is shown as NMDA antagonists, such as ketamine, decrease adrenal loss.  


Excitotoxicity in Neurological Diseases


Because EAATs were discovered to be down-regulated in a variety of central nervous system (CNS) health issues and L-glutamate, as well as L-aspartate, clearance can ultimately affect the excitotoxicity of neurological diseases, many healthcare professionals have decided to determine substances which cause EAAT2, or the main EAAT in the brain and most commonly shown to be downregulated. This has demonstrated substances which shows astrocytic EAAT2 expression both in vitro and in vivo research studies. Several of these have also demonstrated protective properties in animal models of neurological diseases. Cef is one of the most evaluated compounds and it has been analyzed in AD, HD, and ALS models with positive outcomes. However, none of the substances has been extensively researched for its capability to interact with other neuroprotective pathways. Cef has also been demonstrated to promote EAAT2 expression but also to trigger the transcription factor Nrf2, which results in the transcription of a wide array of genes involved in cytoprotection and antioxidant protection. Because oxidative stress is believed to play an essential role in many, if not all, neurological diseases, this pathway may account for the neuroprotection caused by Cef. Furthermore, xCT, which can be one of the downstream targets of Nrf2, has been demonstrated to be upregulated by Cef in vitro and in vivo. Another in vitro EAAT2-promoting substance, MS-153, efficiently protected against secondary neurodegeneration after traumatic brain injury as well as through mechanisms other than EAAT2 upregulation. Evidence of concept experiments which demonstrate the increased stimulation through iGluRs in neurodegenerative diseases needs manipulations of their neurotransmitter physiology.  


Glud1 Tg mice demonstrate a model of excitotoxicity associated with enhanced synaptic L-glutamate activation with restricted neuronal loss. However, this animal model of glutamatergic neurotransmission has not yet been utilized to analyze if Glud1 over-expression aggravates the phenotype of mouse models in neurological diseases. Another version involves the EAAT2-deficient mouse. Homozygous EAAT2 knock-out mice have health issues associated with premature death because of epilepsy as well as hippocampal and focal cortical atrophy. Heterozygous EAAT2 knock-out mice, however, develop normally and show only mild behavioral abnormalities. This mouse model of moderate glutamate hyperfunction has been utilized in a collection of evidence of principle research studies which demonstrated the fundamental role of glutamate. ALS mice, which have both the G93A mSOD1 mutation and a decreased quantity of EAAT2 (SOD1(G93A)/EAAT2±), revealed an increase in the speed of motor decline accompanied by earlier motor neuron loss when compared with single mutant G93A mSOD1 Tg mice. A decrease in survival was also demonstrated in these mutant mice. When crossed with transgenic mice expressing mutations of the human amyloid-β protein precursor and presenilin-1 (AβPPswe/PS1ΔE9), partial loss of EAAT2 unmasked spatial memory deficits in 6-month-old mice expressing AβPPswe/PS1ΔE9. These mice demonstrated an increase in the ratio of detergent-insoluble Aβ42/Aβ40 demonstrating that shortages in glutamate transporter function ultimately cause premature pathogenic processes associated with AD. By comparison, the phenotype of the R6/2 HD mouse model wasn’t changed in mice which had only one EAAT2 allele. Further research studies are still necessary for further evidence.  


As a complement to these research studies, transgenic mice which over-express EAAT2 in astrocytes through the GFAP promoter has also been developed. EAAT2/G93A mSOD1 double Tg mice demonstrated moderate amelioration of their ALS-like phenotype with a statistically significant (14 times ) delay in grip power decrease and loss of motor neurons as well as a decrease in other occasions, such as caspase-3 activation and SOD1, although not at the beginning of paralysis, weight loss or an extended life span when compared with monotransgenic G93A mSOD1 littermates. Exactly the same EAAT2 transgenic mouse model was utilized to evaluate the effect of improved astrocytic L-glutamate and L-aspartate uptake by cross-breeding with an animal model of AD, AβPPswe/Ind mice. Increased EAAT2 protein levels considerably increased and improved overall cognitive functioning, restored synaptic ethics, and decreased amyloid plaques in those AD mice.  


In mice in which genetically engineered regulation and management of xCT causes a lack in the glutamate/cystine antiporter system x−c, the obvious decrease of extrasynaptic L-glutamate is associated with the tremendous resistance of dopaminergic neurons against 6-hydroxydopamine-induced neurodegeneration, perhaps as a consequence of reduced excitotoxicity. However, microglial activation has also been demonstrated to be modulated by system x−c deficiencies leading to a more neuroprotective phenotype which offers an explanation for the protective effect of xCT deletion in this circumstance.  


Therefore, genetic variations encourage the role of chronic excitotoxicity in neurodegenerative diseases, particularly AD and ALS. These models all represent life-long changes in glutamatergic neurotransmission. These models can’t determine if the utilization of drugs and/or medications can directly affect glutamate levels throughout the neurodegenerative process and/or be protective. Both evaluation and analysis of EAAT2-inducing medicine for the progression of inducible mouse models and their interaction with other signaling pathways is still warranted by researchers and healthcare professionals.  


El Paso Chiropractor Dr. Alex Jimenez

In many research studies, evidence and outcome measures have demonstrated that glutamate dysregulation and excitotoxicity in many neurological diseases, including AD, HD, and ALS, ultimately lead to neurodegeneration and a variery of symptoms associated with the health issues. The purpose of the following article is to discuss and demonstrate the role that glutamate dysregulation and excitotoxicity plays on neurodegenerative diseases. The mechanisms for excitotoxicity are different for every health issue. – Dr. Alex Jimenez D.C., C.C.S.T. Insight – Dr. Alex Jimenez D.C., C.C.S.T. Insight



Metabolic Assessment Form


The following Metabolic Assessment Form can be filled out and presented to Dr. Alex Jimenez. Symptom groups listed on this form are not intended to be utilized as a diagnosis of any type of disease, condition, or any other type of health issue.  


  Excitotoxicity is characterized as an acute insult which causes cell death due to the excess activation of iGluRs. Excitotoxicity plays a fundamental role in a variety of central nervous system (CNS) health issues, including cerebral ischemia, TBI, and status epilepticus. The mechanisms for acute excitotoxicity are different for every health issue. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 .  

Curated by Dr. Alex Jimenez   References  

  1. Lewerenz, Jan, and Pamela Maher. “Chronic Glutamate Toxicity in Neurodegenerative Diseases-What Is the Evidence?” Frontiers in Neuroscience, Frontiers Media S.A., 16 Dec. 2015, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4679930/.



Additional Topic Discussion: Chronic Pain

  Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.




Neural Zoomer Plus for Neurological Disease

  Neural Zoomer Plus | El Paso, TX Chiropractor Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual’s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention.  

Formulas for Methylation Support

Xymogen Formulas - El Paso, TX


XYMOGEN’s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.


Proudly, Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.


Please call our office in order for us to assign a doctor consultation for immediate access.


If you are a patient of Injury Medical & Chiropractic Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

  For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download  

* All of the above XYMOGEN policies remain strictly in force.



Again, I Welcome You 👊🏻.

Our Purpose & Passions: I am a Doctor of Chiropractic specializing in progressive, cutting-edge therapies and functional rehabilitation procedures focused on clinical physiology, total health, practical strength training, and complete conditioning. We focus on restoring normal body functions after neck, back, spinal and soft tissue injuries.

We use Specialized Chiropractic Protocols, Wellness Programs, Functional & Integrative Nutrition, Agility & Mobility Fitness Training and Rehabilitation Systems for all ages.

As an extension to effective rehabilitation, we too offer our patients, disabled veterans, athletes, young and elder a diverse portfolio of strength equipment, high-performance exercises and advanced agility treatment options. We have teamed up with the cities premier doctors, therapist and trainers to provide high-level competitive athletes the possibilities to push themselves to their highest abilities within our facilities.

We’ve been blessed to use our methods with thousands of El Pasoans over the last three decades allowing us to restore our patients’ health and fitness while implementing researched non-surgical methods and functional wellness programs.

Our programs are natural and use the body’s ability to achieve specific measured goals, rather than introducing harmful chemicals, controversial hormone replacement, un-wanted surgeries, or addictive drugs. We want you to live a functional life that is fulfilled with more energy, a positive attitude, better sleep, and less pain. Our goal is to ultimately empower our patients to maintain the healthiest way of living.

With a bit of work, we can achieve optimal health together, no matter the age or disability.

Join us in improving your health for you and your family.

It’s all about: LIVING, LOVING & MATTERING! 🍎

Welcome & God Bless


6440 Gateway East, Ste B
Phone: 915-850-0900

East Side:
11860 Vista Del Sol, Ste 128
Phone: 915-412-6677

Clinic Location 1

Address: 11860 Vista Del Sol Dr Suite 128
El Paso, TX 79936
: (915) 412-6677
EmailSend Email

Clinic Location 2

Address: 6440 Gateway East, Building B
El Paso, TX 79905
Phone: (915) 850-0900
EmailSend Email

Clinic Location 3

Address: 1700 N Zaragoza Rd # 117
El Paso, TX 79936
Phone: (915) 850-0900
EmailSend Email

Push As Rx Crossfit & Rehab

Address: 6440 Gateway East, Building B
El Paso, TX 79905
: (915) 412-6677
EmailSend Email

Push 24/7

Address: 1700 E Cliff Dr
El Paso, TX 79902
: (915) 412-6677
EmailSend Email

🔴 Rated Top El Paso Doctor & Specialist by ✔️ RateMD* | Years 2014,2015,2016,2017,2018,2019

Top Rated Chiropractor El Paso

EVENTS REGISTRATION: Live Events & Webinars* ❗️

(Come Join Us & Register Today)

No Events Found

Call (915) 850-0900 Today!