Medical Marijuana has been cited as a controversial topic that has raised debate among supporters and critics. It consists of medicinal Cannabinoids that help treat and manage certain conditions. It is essential to note that Marijuana possesses therapeutic benefits which help in treatment and disease management options. Marijuana contents such as Delta-9-tetrahydrocannabinol and cannabinoids have been cited to support treatment and illnesses management options, posing to have neuroprotective properties. However, medical Marijuana is closely linked with memory and cognition impairments when taken in high doses. It has been pointed to cause short-term memory loss and neurological effects. Marijuana compounds are widely identified with memory and cognition due to their neuroprotective properties encompassing therapeutic potential to treat and manage health conditions. However, it is faced with critics who cite that it can potentially elicit negative neurological impairments.
Medical Marijuana has been cited for slowing and, in some cases, stopping Alzheimer’s disease progression. When an Alzheimer patient is administered low and medically regulated doses of Delta-9-tetrahydrocannabinol helps reduce amyloid-beta plaques in the brain. Delta-9-tetrahydrocannabinol administered doses block amyloid-beta enzymes plaques, boosting the growth of new cells through neurogenesis to facilitate brain damage counteractivity (Calabrese &Rubio-Casillas, P.11). Therefore, medical Marijuana accounts for reduced inflammation agitation and aggression and improved cognitive function.
Cannabinoids contain inflammatory effects that interact with endocannabinoids such as CB1 and CB2 receptors. The receptors are found in the brain, nervous, and immune systems, respectively, to help with inflammation reduction. Furthermore, cannabinoids help modulation immune cell activity by facilitating the production and release of pro-inflammatory molecules, which are vital for minimizing inflammation (Urits et al.). Reduced inflammation helps individuals minimize their physiological response to chronic sensitivity that risks conditions such as multiple sclerosis. Improved cognitive functions are fostered by enhanced endocannabinoid activity in the brain. Endocannabinoid activity accounts for signaling tasks within the brain to help regulate physiological processes such as pain, memory, and mood.
Medical Marijuana also helps reduce Parkinson’s disease symptoms that cause degeneration activities lined with slow movement, imbalance, rigidity, and tremor. Cannabinoids and Tetrahydrocannabinol in marijuana plants contain anxiolytic, analgesic, and Anticon-47 vulsant effects that help with muscle relaxation and antiemetic properties that facilitate counteractivity oxidation of damaged cells and neuroinflammation (Urbi et al., P.2-3). The anti-oxidant properties in cannabis help slow down its interaction with the endocannabinoid system. This helps with neurodegenerative disorder effects management by regulating the body’s motor functions. For example, tremor, a common motor Parkinson’s symptom, is managed by administering cannabis-containing cannabinoid receptor activation features.
The cannabidiols ameliorate the tremor symptom by obstructing the glutamate release and regulating subthalamonigral neuronal overactivity. This helps with movement and basal ganglia regulation responsible for motor control through simulating high frequencies on the subthalamic nucleus. Hence intervention on motor fluctuation and dyskinesias. Dyskinesis is managed by administering cannabinoids which activate CB (1) receptors and block dopamine transporters for dopamine re-uptake (Urbi et al., P.2-3). The cannabinoids CB (1) receptors are found in brain regions at low amounts to model control agents accountable for controlling neurotransmitters’’ levels and activities.
Medical marijuana tetrahydrocannabinol is cited to be an effective option for restoring cognitive function by reducing memory deficits. Cannabis improves synaptic marker protein expression vital for increasing hippocampal spine density. This is especially important in age-related epigenetic approaches reversal. For example, Tetrahydrocannabinol enhances histone acetylation, the hormone responsible for reversing age-related epigone. Cannabis increases histone proteins that accelerate acetyl production and control chromatin DNA packaging. This procedure alters transcription accessibility with other regulatory proteins vital for gene expression management. This implies that epigenetic modification occurs to change chromatin structure fostering cell cycle progression and differentiation. Tetrahydrocannabinol connects with cannabinoids’ brain and body receptors to activate the transcription factors (Calabrese &Rubio-Casillas, P.13).
Low doses of Tetrahydrocannabinol foster the conditioning effect whereby it activates the endogenous compensatory system that helps maintain homeostasis balance (Calabrese &Rubio-Casillas, P.13). This with mitigation of the internal and external challenges such as stress from issues such as injuries and infections. The system produces adrenaline and cortisol, which increase body energy vital for mobilizing the immune system.
Short-term memory loss impedes an individual’s ability to remember and recall information and events. They include cholinergic transmission and acetylcholine synthesis obstruction, and acute intoxication.
Marijuana impedes cholinergic transmission, a part of the central nervous system that influences neuronal growth and survival in the limbic systems and cortex. This is because when a patient is administered the cholinergic antagonist, their muscarinic receptors in the bladder are impaired, resulting in lowered intravesical pressure, causing an increase in blood capacity and reduced bladder contractions (Calabrese &Rubio-Casillas, P.9). Consequently, cholinergic transmission is associated with cognitive issues such as memory loss and confusion that result from obstruction of mental processes such as memory, attention, decision-making, and learning. When Cholinergic transmission is impeded, it causes cognitive dysfunction due to reduced neurotransmitter acetylcholine which has negative implications on the autonomic nervous system, stemming from striated muscle paralysis in the central and peripheral nervous system.
Consequently, Marijuana obstructs acetylcholine synthesis, a vital neurotransmitter in brain functions such as memory, body, and muscle functions (Calabrese &Rubio-Casillas, P.10). The Delta-9-tetrahydrocannabinol minimizes choline in the hippocampus uptake, prompting a decline in neurotransmitters of the acetylcholine that eventually diminishes triggering the hippocampal acetylcholine release effect which blocks acetylcholine syntheses. This is because delta-9-tetrahydrocannabinol hinders the choline transporter’s ability to carry choline into neurons, inhibiting acetylcholine synthesis in memory and cognition. Hence negative implications on the brain trigger cognitive development issues resulting in memory impairment, attention deficits, and mental dysfunctions, prompting short-term memory loss, concentration difficulty, and decision-making and problem-solving impairments.
Chronic use is characterized by acute intoxication, implying total dependence on cannabis, resulting in increased memory and attention impulsivity. When an individual’s impulse rises, they are often susceptible to risky behaviors and poor decision-making. Delta-9-tetrahydrocannabinol binds the cannabinoid receptors, resulting in psychoactive components that disrupt hippocampus functioning, hence impeding memory formation and retrieval (Urits et al.). This is because when an individual smokes Marijuana, the Tetrahydrocannabinol enters the bloodstream and is transmitted to the brain. Hence, acute intoxication occurs when Marijuana is consumed in large doses for a prolonged period, causing an overwhelming on the body to process the large amounts of the cannabinoids.
Neurological effects impair an individual’s nervous system, causing a disorder in its structure and functions, such as Schizophrenia and psychosis (Bhattacharyya et al.). Psychotic effects prompted by medical marijuana point to hallucinations, loss of personal identity, and delusions (Miller et al., P.2). Psychotic disorder has been associated with cannabis and minimal Cannabidiol use due to decreased psycho-activity related to anti-inflammatory and antineoplastic activities. The psychosis-negative induction is triggered by Delta-9-tetrahydrocannabinol adverse effects on the prefrontal cortex (Bhattacharyya et al.). This is because the medical marijuana content causes greater activation of non-salient stimuli, triggering a minimized response to salient stimuli. As a result, the individual experiences ketamine effects, heightening psychotic symptoms induction. Stimulus salience accounts for an individual ability to respond to environmental features that attract attention, such as bright colors, personal identity, and movements.
Schizophrenia is a serious cognitive that distorts people’s interpretation of reality. The condition results in delusions, disordered thinking, and hallucinations. Prolonged use of cannabis worsens schizophrenic symptoms due to its psychoactive property ingredient, Tetrahydrocannabinol. This is because it escalates dopamine activity in the striatum leading to salience attribution (Bhattacharyya et al.). Increased dopamine results in mental health issues such as aggression, poor impulse control, and attention hyperactivity disorder. Consequently, Tetrahydrocannabinol disrupts treatment by obstructing antipsychotic medication treatment effectiveness, commonly used in the treatment of Schizophrenia.
In conclusion, cognitive impairments stemming from marijuana effects relate to frequency, duration, and quantity, thus negatively impacting cognition that impedes functional mechanisms. Medical Marijuana guarantees individuals with neuroprotective effects that protect the brain and nervous system from impairment. Consequently, it enhances cognitive functions through its cannabidiol and tetrahydrocannabinol effect on reducing health conditions such as inflammation and increasing dopamine levels. However, cannabis accounts for short-term memory loss, impairing the ability to carry on with daily living activities. It is also closely associated with psychotropic effects that negatively alter the brain and central nervous systems, interfering with mood, attention, decision-making abilities, and memory. Therefore, it is vital that individuals are cautious and always seek medical guidance for proper and regulated marijuana use. Moreover, individuals must have knowledge of the benefits and risks associated with marijuana use.
Works Cited
Calabrese, Edward J., and Alberto Rubio‐Casillas. “Biphasic effects of THC in memory and cognition.” European journal of clinical investigation 48.5 (2018): e12920.
Urits, Ivan, et al. “Adverse effects of recreational and medical cannabis.” Psychopharmacology bulletin 51.1 (2021): 94.
Urbi, Berzenn, et al. “Effects of cannabis in Parkinson’s disease: a systematic review and meta-analysis.” Journal of Parkinson’s Disease 12.2 (2022): 495-508.
Bhattacharyya, Sagnik, et al. “Induction of psychosis byδ9-tetrahydrocannabinol reflects modulation of prefrontal and striatal function during attentional salience processing.” Archives of general psychiatry 69.1 (2012): 27-36.
Miller, Norman S., Redon Ipeku, and Thersilla Oberbarnscheidt. “A review of cases of marijuana and violence.” International journal of environmental research and public health 17.5 (2020): 1578.
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