Risk Factors

In the contemporary healthcare, anyone is susceptible to acquiring PTSD at any age. According to the research conducted by Otis, Marchand, and Courtois (2012) indicates the prevalence of PTSD persons are varying between 7 percent and 44 percent. The difference in the number is associated with the changes and variability observed in these studies. On the other hand, the above statistics are important in studying PTSD and the associated risk factors in different persons (Otis, Marchand, and Courtois, 2012). Furthermore, other research indicated that women are more likely to acquire PTSD than men, in the sense that gene and immune re the difference in both of them. Women are more likely to develop PTSD than men, and genes may make some people more likely to develop PTSD than others. Other risk factors that may be characterized by with PTSD include pre-traumatic factors that comprise of the characteristics of the individual that was present before the traumatic event.

Below are some of the factors that should be considered when it comes to the understanding of the risk factors for PTSD.

Why do some people develop PTSD and other people do not?

According to the emphasis relayed by Mike Membrino on the understanding of the PTSD, he posits that is significant to acknowledge that everyone can acquire PTSD regardless of the race, religion, or ethnicity. In this case, several risk factors might increase the rate at which a person might develop PTSD. Separately, scientific research indicates that other individuals cannot develop this mental disorder regardless of the nature of the risk factors.
Michael Membrino, President of Neuro-Endoceuticals, also notes that several factors play vital role when it comes to the development of PTSD. A comprehensive list below is summarized by Aswin Suri and his colleagues, to understand both various risk and reliance factors that are connected to PTSD.
Risk Factors and Resilience Factors for PTSD
When it comes to the development of PTSD, below are the risk factors:
· Disasters caused by human error.
· Victims of rape or sexual assaults.
· Living through dangerous events or traumas.
· Those diagnosed with life-threatening illness.
· Combat veterans.
· Dealing with extra stress after events such as loss of the loved one’s ones, pain of injury or loss of job or mortgage.
· Little or no social support that makes individual feel isolated.
Some of the resilient factors that may reduce PTSD include:
· Getting social support from people and other family friend will create happiness.
· Participating in event such as traumatic events.
· Understanding and practicing the effectiveness in feeling good.
· Having positive though bout people opinion and learning how to get along.
· The essence of managing fear, depression, and anxiety will help the situation.
· Learning and adopting strategies of forgetting the bad events that might have led to trauma events.
Additionally, following the research conducted by Iversen et al. (2008) understanding the factors which increase and reduces the risk of PTSD is very important when it comes to its management. In their findings, they realized that the primary PTSD symptoms are associated with lower ranks in office, being un married, having less education in the military camp, and history of childhood adversity or victimizations (Iversen et al., 2008). Therefore, taking into considerations of these factors, it is suggested that possible solution towards PTSD will emerge in the near future.References:
Iversen, A. C., Fear, N. T., Ehlers, A., Hughes, J. H., Hull, L., Earnshaw, M., & Hotopf, M. (2008). Risk factors for Post-Traumatic Stress Disorder amongst United Kingdom Armed Forces personnel. Psychological Medicine, 38(4), 511–522.

Otis, C., Marchand, A., & Courtois, F. (2012). Risk Factors for Posttraumatic Stress Disorder in Persons With Spinal Cord Injury. Topics in Spinal Cord Injury Rehabilitation, 18(3), 253–263.



The Role of Neuron Creation in Anxiety Disorders



According to Mike Membrino, anxiety and stress disorders are among the major prevalent of PTSD.

Separately, the clinical manifestations of these disorders provide a spectrum of alterations. To some extent, the present original trauma effects and when untreated, the disease can develop a significant impairment in functioning, reduced quality of life, and enormous economic burden. Recent studies have examined the underlying literature review on the neural mechanism when regulating impaired pattern present in anxiety.

According to the note submitted by Rene Hen, Ph.D., of Columbia’s Department of Psychiatry and the NY Psychiatric Institute, suggest that the production of the neuron or the in the brain have assisted in the treatment of anxiety that is associated with PTSD (Duval et al., 2015).
They further note that the thalamus is an implicated sensory integration. In effect, through activation, the thalamus is associated with high degree of anxiety and disgust in blood-injury-injection phobia, as well as automatic arousal in snake phobia. In the treatment with paroxetine reduces the activation of the thalamus, therefore, tend to reduce anxiety. Additionally, in the hippocampus, the dentate gyrus that is that separate is among the two areas of the brain where neurogenesis takes place. Among the possible improving patterns separation is the addition in the number of adult-generated neurons, so they are better able to process information. Besides, there is enough evidence that shows that reduced hippocampal can be achieved through functional neuroimaging.
Moreover, recent studies provide that in the current models of PTSD, hypoactivity in frontal regions suggests a reduced potential for top-down regulation of fear and fear extinction (Holzschneider & Mulert, 2011). The hippocampus provides information about the context of a situation, and the attenuated hippocampal response might be attributable to difficulties in identifying safe circumstances (Holzschneider & Mulert, 2011). Besides, the above mentioned functional modalities in the brain, including the hippocampus, amygdala, and medial prefrontal cortex, have shown possibilities in the patients with PTSD (Holzschneider & Mulert, 2011).
Therefore, the studies as mentioned earlier researchers emphasize on the using better use of technological advancement in imaging. Finally, research should be conducted on patient with impairments in pattern-separation tasks and decreased neurogenesis in the dentate gyrus.


Holzschneider, K., & Mulert, C. (2011). Neuroimaging in anxiety disorders. Dialogues in Clinical Neuroscience, 13(4), 453–461.

Duval, E. R., Javanbakht, A., & Liberzon, I. (2015). Neural circuits in anxiety and stress disorders: a focused review. Therapeutics and Clinical Risk Management, 11, 115–126.


PTSD Treatment Modalities

PTSD Treatment Modalities
Treatments and Therapies
When it comes to the treatment and management of PTSD modalities, some research indicated that medications for psychotherapy are the primary methods that should be adopted, based on their argument of fact that every individual is different from one another and therefore, treatment should be suggested differently. Additionally, it is important for anyone with PTSD to be treated by a mental health provider who is experienced with PTSD as presented by Michael Membrino, President of Neuro-Endoceuticals. According to the Committee on the Assessment of Ongoing Effects in the Treatment of Posttraumatic Stress Disorder; Institute of Medicine. Treatment for PTSD in Military and Veteran Populations (2007). The vast majority treatment of PTSD includes psychological therapies. This procedure includes exposure therapies, stress inoculation training, and cognitive therapies.
PTSD Treatment Modalities
One of the most pharmacotherapy used in the treatment of PTSD is the use of antidepressants. For example, the use of Tricyclicsand Monoamine Oxidase Inhibitors is said to be more efficient in the sense that they assist ins restoring sleep and pain other antidepressants such as Nefazodone has been found to be of greater benefit in the study of US veterans. Most of the time, medications do not eliminate symptoms but provide symptom reduction and could be more efficient when used in conjunction with an ongoing program of trauma specific psychotherapy for patients, such as PE or CPT (14).Monotherapy trials of uncharacteristic antipsychotic therapy versus placebo have yielded mixed results. They include a small negative trial of olanzapine in veterans and two partially ongoing research of risperidone in women who had PTSD originating from childhood abuse. Quetiapine was found to be superior to placebo in a two-site is useful in the management trial of 80 veterans who had PTSD (Committee on the Assessment of Ongoing Effects in the Treatment of PTSD, 2007).


This is another method that can be used to treat PTSD. For example, the use of exposure therapies to reduce PTSD symptoms is associated with reducing problems such as anxiety, depression, fear that helps these patients to confronts their trauma-related issues like memories and feelings.
Exposure therapies interventions entail exposing to the image of repeated revisiting of the traumatic memory, which makes the feared situations compromised. Research shows that general family support and social awareness supports the recovery of the patient (Committee on the Assessment of PTSD, 2007).
Another method that is used to treat PTSD is cognitive therapies. According to Mike Membrino, this CT is a treatment procedure in which the systems assist the patient to ignore negative thoughts and help the understand the pathologic emotions and behaviors. In this case, cognitive therapies have been reported to be useful in the management of the PTSD.

How Talk Therapies Help People Overcome PTSD

This is another way that has been adopted by a clinician to assist in the treatment of PTSD. Talk therapies are essential in the sense that they empower the treatment of PTSD through various actions and knowledge that is achieved through civic education. Based on this general goal, different types of therapy may:

~ Education on trauma management therapy will assist the patient with PTSD to withdraw from expression of anger, and interpersonal difficulties. The therapy combines intensive individual exposure therapy, programmed practice, and structured social and emotional skills training groups.
~ Educate about trauma and it effect, symptoms and basically how it can be prevented.
~ Use skill such as relaxation and anger-control in order to seek attention of the patient.
~ Teach the patient how to manage their anger, deal with shameful situations and support trauma incident reduction.
~ Examine the reactions of the patient with specific medication and understand what procedures should be taken for medical follow ups.References:

Committee on the Assessment of Ongoing Effects in the Treatment of Posttraumatic Stress Disorder; Institute of Medicine. Treatment for Posttraumatic Stress Disorder in Military and Veteran Populations: Initial Assessment. Washington (DC): National Academies Press (US); 2012 Jul 13. 7, Treatment. Available from:



Beyond Treatment: How can I help myself?
Up to the present times, most of the national hospital institution re currently engaging in clinical interventions that are associated with prevention and strategies on how to manage PTSD. Mike Membrino, President of Neuro-Endoceutials notes the contemporary medical and healthcare setting should participate in various research and clinical trials that would assist in the management of PTSD. In this case, there exists some procedure that every individual should focus on when it comes to the management of related mental disorder. Additionally, Mike Membrino further suggests that these clinical interventions are beyond treatment and they are significant even though they cannot be quickly adopted by a patient of the related disease. The central objective of how a person should assist themselves when it comes to the management of similar mental disorder is to seek medical doctor’s advice and prescription. On the other hand, Michael Membrino, President of Neuro-Endoceuticals, argues that patients are also guaranteed to check with the National clinical practice guidelines that would provide necessary procedure on the best course of action in dealing with post-traumatic stress disorders.Mike Membrino, also suggest that any patient with mental illness should be provided with emergency care in that every nursing or clinician should be able to provide temporary care and further instruction on how the patient can receive further help in the management of the disease before seeking the actual treatment. In this case, the Neuro-Endocueitcals Team suggest that an individual with PTSD should take the following course of action to help themselves.

· Participate in physical activities that would promote the functioning of the body
· Individuals should also primary and realistic goals
· Engage in whatever you can do at the moment. Push large tasks ahead.
· Take your time around and socially interact with other individual to get the overall experience.
· Always stay positive and send good thoughts to the universe, for example have the hope that your symptoms will improve momentarily.
· Seek comfort and family support to keep your moods precisely.

Consequently, in the modern health care setting, the value of caring for oneself is a significant aspect when it comes to a large number of individuals exposed to traumatic events. In this case, this article presents further information and understanding the research and clinical trials on PTSD.

Next Steps for PTSD Research

According to the analysis provided by Mike Membrino, President of Neuro-Endocueticals, PTSD is among the most common mental health disorders in the United States. In his manuscripts, Suri reviews that the epidemiology and clinical manifestations of the PTSD suggest that the disease has only screening, treatment, and directions in the PTSD research are the only options remaining. Separately, various recent studies showcase progress in the research on the mental and biological foundation of the PTSD, which had made most of the scholars and scientist to dwell on the clear understanding of the symptoms that are associated with trauma. This is because patients with trauma present a spectrum of reactions. Some of the recent research in understanding PTSD are presented below:
· Research conducted by Lancaster, Cynthia L. et al. (2016) suggest that exposure-based interventions are the most empirically supported treatment modalities of the PTSD.
· The NNIMH- have funded a team of researchers in the investigation of the trauma patients in acute care in order to acknowledge the changed that occurs in individuals whose symptoms improves naturally.
· Other recent studies studying the clinical implementation of the preventive interventions and how this provision of specialized treatment are adjusting the symptoms of the patient with trauma (Qi, Gevonden, & Shaley, 2016).
· Other researchers are being conducted to examine several factors that might indicate whether individual with PTSD care able to positively responds to various types of clinical interventions.
Qi, W., Gevonden, M., & Shalev, A. (2016). Prevention of Post-Traumatic Stress Disorder After Trauma: Current Evidence and Future Directions. Current Psychiatry Reports, 18, 20. , C. L., Teeters, J. B., Gros, D. F., & Back, S. E. (2016). Posttraumatic Stress Disorder: Overview of Evidence-Based Assessment and Treatment. Journal of Clinical Medicine, 5(11), 105.

Join a Study

What are Clinical Trials?
According to the explanation provided by Mike Membrino, Clinical Trials are research studies that are set in place to explore whether the medical strategy, treatment, or interventions can safely and efficiently solve the problem, in this case, Neurodegeneisis disorders. On the other hand, Umscheid, Margolis, & Grossman (2011) argue that clinical trials in their purest nature, are designed to observe outcomes of the human subjects under experimental conditions by the researchers or scientist. In this study, clinical trials will tend to focus on the effectiveness and safety of the interventions towards PTSD. Additionally, it is argued that a clinical trial is necessary for the sense that it permits the randomization of the intervention, thereby effectively removing the section bias that results from the imbalance of the unknown (Umscheid, Margolis, & Grossman (2011). Finally, for a trial to precisely address the primary objective, a sufficient sample size is required to have complete power in being able to detect a possible statistical difference.References:

Umscheid, C. A., Margolis, D. J., & Grossman, C. E. (2011). Key Concepts of Clinical Trials: A Narrative Review. Postgraduate Medicine, 123(5), 194–204.


ALCAR Neuroprotection and Pro-Neurogenic Effects


ALCAR is reported to be a naturally occurring substance that, when used or administered at supraphysiologic concentrations, is neuroprotective in various models of focal cerebral ischemia.


ALCAR Neuroprotection and Pro-Neurogenic Effects

On the other hand, oxidative stress and neuroinflammation are the central factors that cause progressive degeneration of dopaminergic neurons in Parkinson’s disease.

The neural stem cells, on the other hand, underwriters in maintaining brain plasticity; hence, survival of neural stem cells and neuroblast in the process of the neurodegenerative process becomes significant in refilling the puddle of established neural population. And because ALCAR is present in almost all the body cells, it heightens endogenous antioxidants and regulates biogenetics.

In the contemporary medicine and healthcare setting, there is no evidence suggesting the putative mechanism and neuroprotective effects of ALCAR in 6-OHDA induced rat and mode of PD-like phenotypes. In this case, we examined the impact of ALCAR on death/survival of dopaminergic, neuroblast, and NSCs and the associated mechanism of the neuroprotection in 6-OHDA rat of PD-like phenotypes. In the diagnosis process, using ALCAR (100 mg/kg/day, intraperitoneal (i.p.)) treatment began three days earlier to 6-OHDA lessening and proceeded for another fourteen-day post-lessoning (Levy et al., 2009). From the lab result, it was discovered that the pre-treatment of ALCAR in 6-OHDA-lesioned rats increased the expression of the neurogenic and the pathway genes in the striatum and substantia nigra pars compacta (SNpc) region.
Separately, exposure of the cultured neural cells to ALCAR inhibits apoptosis caused by the deprivation of serum. Besides, it was discovered that the pretreatment using ALCAR in 6-OHDA-lesioned reduced GSK-3β stimulation and amplified nuclear translocation of β-catenin. Purposeful deficits were reestablished subsequent ALCAR pretreatment in 6-OHDA-lesioned rats as established by the better-quality motor organization and revolving behavior, authorizing fortification of DAergic innervations in lesioned striatum (Singh et al., 2017). In conclusion, the overall result of the investigation suggests that ALCAR exercises exclusive neuroprotective effects through the stimulation of β-catenin pathway, telling its beneficial use to treat neurodegenerative sicknesses by improving reformative capability and subsequently neuroprotection.References
Levy, O. A., Malagelada, C., & Greene, L. A. (2009). Cell death pathways in Parkinson’s disease: proximal triggers, distal effectors, and final steps. Apoptosis : An International Journal on Programmed Cell Death, 14(4), 478–500.

Singh, S., Mishra, A., Mishra S, & Shukla, S. (2017). ALCAR promote adult hippocampal neurogenesis by regulating cell-survival and cell death-related signals in rat model of Parkinson’s disease like-phenotypes. 108:388-396. doi: 10.1016/j.neuint





Acne Treatment
Past research has suggested that certain cannabinoids like CBD can reduce symptoms of acne. This discovery led researchers to investigate whether other non-psychoactive cannabinoids may be beneficial in treating acne disorders.

A 2016 study found that CBC was particularly useful as it reduced the production of sebum by sebaceous glands, which causes symptoms of acne. CBC was also found to reduce the effects of arachidonic acid, which plays a major role in acne production.
These effects, coupled with the ability of CBC to reduce inflammation, led the researchers to conclude that CBC may be “highly efficient” as an anti-acne treatment.

A 2012 study investigated the potential for CBC to manage bowel hypermotility, also known as diarrhea.
The researchers discovered that CBC reduced inflammation-induced hypermotility without causing hypo motility, or constipation.
This suggests that CBC may be a better treatment for diarrhea, since many current anti-diarrheal medications are known to cause constipation.

Bone Growth
CBC may also play a role in regulating bone growth. Scientists have found that low concentrations of cannabinoids can activate cells that are responsible for bone growth and repair, known as osteoclasts.
While CBC specifically has not yet been investigated by researchers in this function, other cannabinoids have demonstrated very promising potential in contributing to bone growth and repair through their activity on the CB2 receptor.
This notion can be expanded to include CBC since it activates the CB2 receptor indirectly and also increases levels of endocannabinoids, which act to enhance osteoclasts.

Cannabinoids have been found to display various anti-cancer properties in a number of studies. One of these properties involves the ability of cannabinoids to induce apoptosis in cancer cells, which is a programmed cell death response.
Another anti-cancer property of cannabinoids involves the ability of this class of chemicals to block cancer cells from proliferating. This means that the ability of cancer cells to divide in order to grow and expand can be inhibited by cannabinoids.
However, studies have not investigated the role of CBC specifically in producing anti-cancer effects.
But CBC’s indirect activity on the CB2 receptor, as well as its ability to influence the activity of endocannabinoids such as 2-AG and anandamide, suggest that CBC may contribute to the anti-cancer properties of Hemp Extract.

One of the earliest studies involving cannabichromene was published in 1981 by researchers at the University of Mississippi.
In the study, researchers found that CBC exhibited “strong” antibacterial effects on a variety of gram-positive and gram-negative bacteria, including E. coli and staph (S. aureus).
CBC showed “mild to moderate” activity against different types of fungi too, including a common food contaminant known as black mold.
Recent animal studies show CBC can reduce edema (swelling) as well as inflammation of the intestinal tract.
Interestingly, CBC appears to fight inflammation without activating cannabinoid receptors. This could explain why CBC produces a stronger anti-inflammatory effect when combined with other cannabinoids like THC.

Pain Relief
Cannabichromene has also been found to reduce pain in animal models, although its effect may not be as strong as THC.
However, a 2010 study concluded that CBC and CBD could both fight pain by “interacting with several targets involved in the control of pain” at the spinal level.
Since CBC and CBD are both non-psychoactive, scientists are hopeful that these Hemp Extract compounds can be used to treat pain without causing a high.

a 2010 study from the University of Mississippi identified a significant antidepressant effect of CBC in rat models.
The researchers concluded that CBC along with other cannabinoids including THC, CBD, CBN and CBG may “contribute to the overall mood-elevating properties of hemp.”

Recent studies on CBC have led to the discovery of a very unique benefit — it may actually help promote the growth of new brain cells. Specifically, CBC appeared to increase the viability of developing brain cells, a process known as neurogenesis.
Contrary to popular belief, the brain doesn’t stop growing once you reach a certain age. However, neurogenesis in adults only occurs in a specific part of the brain called the hippocampus.
While CBC’s ability to promote neurogenesis is a very recent finding, previous studies have suggested that CBD might do the same.
As Dr. Xia Jiang of the University of Saskatchewan — one of the first scientists to uncover this remarkable effect — explained in an interview with Science Daily:
“Most ‘drugs of abuse’ suppress neurogenesis. Only hemp extract promotes neurogenesis.”
Opiates, alcohol, nicotine, and cocaine are all known to inhibit brain growth. Yet CBC and other chemicals in hemp extract appear to have the opposite effect.


Where do I buy Bulk CBD Hemp Oil Wholesale


Interested in buying Bulk CBD Oil or becoming a Wholesale CBD Hemp Distributor?

Where do I buy Bulk CBD Hemp Oil Wholesale


We have a money back guarantee (backed by lab results) on our prices and with our buying power of raw and finished products for sale so we can pass the savings onto our clients.  Click here for  ONLY Kentucky Bulk CBD Oil Wholesale (Hemp only)

Where do you go to buy wholesale CBD Oil? We know we have the finest caliber of CBD Hemp Oil at the lowest prices. We are so confident that we post our prices. Our primary CBD is full or broad spectrum CBD Oil. However, we carry Isolate or crystals as well who wish to formulate their own products, but please don’t assume that you will get THC if you don’t use Isolate or crystals. We encourage all non-formulating distributors to use our Full Broad Spectrum Oil which is proven to more effective than isolated CBD crystals. Email us TODAY at CBD Oil For Sale


We sell the finest Full Spectrum Oil grown locally here in the USA. Depending on the volume of your current oil or future purchases, we have extremely competitive prices; especially if a supply agreement with minimum thresholds are accomplished:


As of Jan 2017, the following wholesale Cannabinoid Oil prices are in existence. This is not a full list of CBD bulk wholesale prices, but one which gives a basic price idea. Prices are subject to change without notice. Minimum orders & Supply agreements in effect:

bulk 2.5 cents/mg OR $25,000 per kg; 3 grams, 10 grams, 100 grams & 1 to 50 kgs

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Why is our CBD different than the best CBD out there? It isn’t! but what???

Then why is your CBD so effective.
It’s all in BIOAVALABILITY.   The way to understand this properly is the Human body allows some molecules and substances to enter the blood stream more effectively than others based on certain properties of those respective molecules. Our CBD under goes ONE extra step of proprietary refining prior to leaving our facilities in order to ensure that we have the BEST CBD in the world.

Where is Cannabidiol Found?

Cannabidiol is produced in 2 ways:
Naturally, in the cannabis plant. Cannabidiol can be found in both hemp and marijuana varieties of cannabis. The main functional difference between hemp and marijuana is the level of THC. Marijuana is grown specifically to contain significant levels of THC – usually for recreational use, while hemp has only trace amounts of THC. CBD found naturally in hemp is also legal in the United States (like all other hemp imports), while CBD from marijuana is federally illegal in the United States, though state-by-state legalization is occurring rapidly.

Cannabidiol can also be produced synthetically in a laboratory. However, synthetically produced cannabidiol is a regulated substance, and possession of it is legal outside of few specialized circumstances.

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Alzheimer’s Disease


Speeding Brain’s Garbage Disposal Could Slow Alzheimer’s


In the modern neurodegenerative care, scientists have been on the merge in determining the way of treating diseases associated with the brain.

Recent researchers from the role of endocannabinoids to cannabinol have proven the possibility of regulating neurogenesis disorders as asserted by Mike Membrino of Neuro-Endoceuticals, USA. On the other hand, recent studies have found that using drugs to boost the activity in the brain “garbage disposal” has the potential of removing the toxic protein that clumps together in the brain to cause Alzheimer’s disease. Consequently, Michael Membrino, President of Neuro-Endoceuticals, USA, argues that most of the neurological disorder such as AD is characterized by the accumulation of protein in the brain, which will result into various tauopathies. Research conducted by Feunerburk, Marcellino, and Yue (2010) found that overexpression of protein accumulation in the brain has resulted in various autophagy dysfunction. In their investigation, they discovered that the use of different depressant to boost brain through activation of garbage disposal system slows down the disease in mouse model.

           However, in the study, the team posted that use of different animals, cellular models, and experimental paradigm may provide distinct differences in conclusions (Feunerburk, Marcellino, and Yue, 2010). Similarly, research conducted by scientists from the University of Columbia have been reported new ways of activating brain garbage disposal system can reduce the prevalence of Alzheimer’s disease. As reported by Karen Duff, the team leader of the research group, use of drugs to increase or speed up the brain garbage disposal system is beneficial in the sense that it open new interventions for treating the disease and several other neurogenesis disorders (Dockrill, 2015). Focusing on the nature of protein accumulation in the brain, the cells of the brain tend to clear off the dead cells and replace them with new ones. Because these damaged protein cells may sometimes be sticky, for example, amyloid beta and tau proteins, they clot or stick together and contribute to the development of Alzheimer’s disease.
           In the study, the team used mouse models and administered rolipram that is an antidepressant to the mice. In their result, they discovered that the level of the toxic protein in the brain of the mice was reduced the positive effect. In their explanation, rolipram activated proteasome and restored the protein disposal to normal levels. Additionally, the drug was associated with the improved memory of the mice, but this was unclear (Dockrill, 2015). Following the recent study, it was discovered that the mechanism to which rolipram works is through the inhibition of the PDE-4 enzyme, which can increase the activity of proteasome within the brain. On the other end, accumulation of the protein in the brain is connected to reduce peptidase activity, which leads to high levels of ubiquitinated proteins. The potential interference of dysfunctional tau with autophagosome clearance may lead to AD neuropathology.
           This is possible because tau has have been reported to control the stability or microtubules; hence, the modification of tau can lead to stabilization of the condition. Consequently, it was possible that the researchers were able to activate proteasome, which resulted in the reduction of the tau and improvement in memory function of the mice, it was still on how the anti-depressant worked. Besides, clinical manifestation shows that rolipram can cause nausea and the drug is not advised to be administered to human beings. In effects, the researchers reported that they have no idea of how the rolipram was able to activate the proteasome and regulated the protein accumulation in the brain.
           However, it was apparent that the team was able to understand and discover that use of some drugs, in this scenario, rolipram was able to stimulate this disposal system in neurons and efficiently reduces the Alzheimer’s disease. In this light, there is a potential in new interventions of Alzheimer’s disease and other neurodegenerative illnesses. In conclusion, Aswin Suri, Chairman of the Neuro-Endoceuticals and his colleague Mike Membrino, President of Neuro-Endoceuticals, USA, assert that drugs that may act in activation of proteasome can be used to assist in the management of the AD and other protein based accumulation diseases such as Parkinson’s disease, Huntington’s disease, and frontotemporal dementia.
Dockrill, P. (2015). Drug that Boost the Brain’s “Garbage Disposal” Slows Alzheimer’s in Mice. Colombia University Medical Care. Funderburk, S. F., Marcellino, B. K., & Yue, Z. (2010). Cell “Self-Eating” (Autophagy) Mechanism in Alzheimer’s Disease. The Mount Sinai Journal of Medicine, New York, 77(1), 59–68.