CT Scans Reveal Acupuncture Points

Expectancy effects in the Autonomous Sensory Meridian Response

Autonomous Sensory Meridian Response Functional Connectivity

Plasticity of amyloid fibrils

Amyloid fibrils appear to more resemble plastic materials generated from synthetic polymers than they do globular proteins.

A central conundrum of the amyloid phenomenon is the ability of highly evolved polypeptide sequences, to fold into a form stable, fibrillar, cross-ß amyloid structures.

Understanding how different polypeptide sequences can fold into a cross-ß has been one of the challenges of the amyloid field.

Interestingly, synthetic polymer assemblies often exhibit a similar isomorphism.

Basic text on plastics reads remarkably like a summary of the recent discovery of multiple conformations of amyloid fibrils.

Capillaries scramble to feed oxygen to brain

Tiny bleeds raise disability risk for people with MS

central nervous system



brain injury

spinal injury






conditioned fear


amyotrophic lateral sclerosis

multiple sclerosis




Cannabinoids and cell fate.

Conclusion: The experimental evidence indicates that cannabinoids protect normal neurons from toxic insults.

Control of the cell survival/death decision by cannabinoids.

Cannabinoids and cell fate.Conclusion: Regarding the central nervous system, most of the experimental evidence indicates that cannabinoids may protect neurons from toxic insults such as glutamaergic overstimulation, ischemia and oxidative damage.


Neuroprotective antioxidants from marijuana

Conclusion: The psychotropic cannabinoid receptor agonist Δ9tetrahydrocannabinol (THC) and cannabidiol, (a non-psychoactive constituent of marijuana), both reduced NMDA, AMPA and kainate receptor mediated neurotoxicities.

Δ9-tetrahydrocannabinol protects hippocampal neurons from excitotoxicity.

Conclusion: Excitotoxic neuronal death underlies many neurodegenerative disorders. This study demonstrates the importance of agonist efficacy and the duration of treatment on the neuroprotective effects of cannabinoids.

Tetrahydrocannabinol in a method of treating glaucoma

Neuroprotective Effect of Δ9-Tetrahydrocannabinol and Cannabidiol in N-Methyl-d-Aspartate-Induced Retinal Neurotoxicity

Conclusion: In glaucoma, the increased release of glutamate is the major cause of retinal ganglion cell death. In conclusion, our results indicate that lipid peroxidation and ONOO- formation play an important role in NMDA-induced retinal neurotoxicity and cell loss in the retina, and that THC and CBD, by reducing the formation of these compounds, are effective neuroprotectants.

Inhibition of tremulous jaw movements in rats by memantine-Δ9 -tetrahydrocannabinol combination: neuroanatomical correlates

Memantine and Δ9 -tetrahydrocannabinol alone were without effect, however, co-administration of the drugs significantly decreased number of haloperidol-induced jaw movements. The antitremor activity of the combination was antagonized (i) by injections of L-glutamate into the dorsal striatum, entopeduncular nucleus, substantia nigra pars reticulata, globus pallidus, supratrigeminal and trigeminal motor nuclei but not into the subthalamic and cuneiform nuclei; (ii) by injections of CGS 21680 into the ventrolateral striatum; (iii) by injections of bicuculline into the rostral part of the parvicellular reticular nucleus. The presented results identify brain areas influencing parkinsonian-like tremor in rats; these data can help advance the development of novel treatments for repetitive involuntary movements.


Neurocognition in college-aged daily marijuana users

Conclusion: Marijuana users were high functioning, demonstrating comparable IQs to controls and relatively better processing speed. Marijuana users demonstrated relative cognitive impairments in verbal memory, spatial working memory, spatial planning, and motivated decision making but comorbid use of alcohol, which was heavier in marijuana users, was unexpectedly found to be associated with better performance in some of these areas.

Is Illicit Drug Use Harmful to Cognitive Functioning in the Midadult Years?

Conclusion: At the population level, it does not appear that current illicit drug use is associated with impaired cognitive functioning in early middle age.

Effects of Smoking Marijuana on Brain Perfusion and Cognition

Smoking marijuana resulted in intoxication, as assessed by a behavioral rating scale, but did not significantly alter mean behavioral performance on the attention task. There was no significant rCBF change in the nucleus accumbens or other reward-related brain regions, nor in basal ganglia or hippocampus, which have a high density of cannabinoid receptors.

Intelligence, cognition unaffected by heavy marijuana use

Conclusion: The observers conclude that heavy marijuana use produces no irreversible mental deficits.

Preliminary findings of a longitudinal study of effects on IQ in young adults

Conclusion: We conclude that marijuana does not have a long-term negative impact on global intelligence.

Long-term effects of marijuana use on the brain

Conclusion: Compared with controls, marijuana users had significantly less bilateral orbitofrontal gyri volume, higher functional connectivity in the orbitofrontal cortex (OFC) network, and higher structural connectivity in tracts that innervate the OFC (forceps minor) as measured by fractional anisotropy (FA)

stimulate brain cell growth

Role of cannabinoids in Neurogenesis

Cannabinoids Regulators Neurogenesis

Cannabinoids Reduce Alzheimer' Proteins

Prevention of Alzheimer' Disease Pathology by Cannabinoids:
Neuroprotection Mediated by Blockade of Microglial Activation

Targeting the Endocannabinoid System in Alzheimer' Disease

Multitarget cannabinoids as novel strategy for Alzheimer disease

Cannabinoids for the Treatment of Agitation and Aggression in Alzheimer' Disease

Long-term cannabidiol treatment prevents development of social recognition deficits

Prevention of Alzheimer' disease pathology by cannabinoids

The endocannabinoid system and Alzheimer' disease

Therapeutic effects of THC on Alzheimer' disease

Cannabinoids for treatment of Alzheimer' disease

Research Suggests Marijuana Analogue Stimulates Brain Cell Growth

Conclusion: The team found that rats treated with HU-210 on a regular basis showed neurogenesis – the growth of new brain cells in the hippocampus. This region of the brain is associated with learning and memory, as well as anxiety and depression. The effect is the opposite of most legal and illicit drugs such as alcohol, nicotine, Heroin™, and cocaine.

Mechanisms of cannabidiol neuroprotection

Conclusion: Our findings demonstrate that CBD exerts robust neuroprotective effects in vivo in HI piglets, modulating excitotoxicity, oxidative stress and inflammation, and that both CB2 and 5HT1A receptors are implicated in these effects.

The anxiolytic effect of cannabidiol on chronically stressed mice depends on hippocampal neurogenesis

Conclusion: Cannabidiol (CBD), the main non-psychotomimetic component of the plant Cannabis sativa, exerts therapeutically promising effects on human mental health such as inhibition of psychosis, anxiety and depression. However, the mechanistic bases of CBD action are unclear. Here we investigate the potential involvement of hippocampal neurogenesis in the anxiolytic effect of CBD

Role of cannabinoids and leptin in neurological diseases

Cannabinoids exert a neuroprotective influence on some neurological diseases, including Alzheimer', Parkinson', Huntington', multiple sclerosis and epilepsy. Cannabinoids may exert effects via a number of mechanisms and interactions with neurotransmitters, neurotropic factors and neuropeptides.

Leptin is a peptide hormone involved in the regulation of food intake and energy balance via its actions on specific hypothalamic nuclei. Leptin receptors are widely expressed throughout the brain, especially in the hippocampus, basal ganglia, cortex and cerebellum. Leptin has also shown neuroprotective properties in a number of neurological disorders, such as Parkinson' and Alzheimer'.

do you have a backbone?

Protective Effects of Cannabidiol on
Lesion-Induced Intervertebral Disc Degeneration

CB1 cannabinoid receptor agonist inhibits matrix
metalloproteinase activity in spinal cord injury

spinal injury

Cannabinoids to treat spinal cord injury.

Conclusion: The endocannabinoid system is expressed in the intact spinal cord, and it is dramatically upregulated after lesion.

Protective effects of cannabidiol on lesion-induced intervertebral disc degeneration

Conclusion: Considering that cannabidiol presents an extremely safe profile and is currently being used clinically, these results suggest that this compound could be useful in the treatment of intervertebral disc degeneration.

Cannabinoids and bone regeneration

Effect of marijuana use on outcomes in traumatic brain injury.

Conclusion: The THC(+) group was compared with the THC(-) group with respect to injury mechanism, severity, disposition, and mortality. A positive THC screen is associated with decreased mortality in adult patients sustaining TBI.

Cannabinoid agonist rescues learning and memory after a traumatic brain injury

Conclusion: We found that the brain-injured animals treated with the agonist showed a marked recovery.

An endogenous cannabinoid (2-AG) is neuroprotective after brain injury.

Conclusion: When 2-AG was administered together with additional inactive 2-acyl-glycerols that are normally present in the brain, functional recovery was significantly enhanced.

Ultralow doses of cannabinoid drugs protect the mouse brain from inflammation-induced cognitive damage

Conclusion: An ultralow dose of THC that lacks any psychotrophic activity protects the brain from neuroinflammation induced cognitive damage and might be used as an effective drug for the treatment of neuroinflammatory conditions, including neurodegenerative diseases.

The effect of cannabichromene on adult neural stem/progenitor cells

Conclusion: Our results suggest that CBC raises the viability of NSPCs while inhibiting their differentiation into astroglia, possibly through up-regulation of ATP and adenosine signalling.


Cannabis May Help Reduce Brain Damage Caused By Ischemic Strokes

A recent meta-analysis of 144 animal studies including 1,473 subjects (rats, mice, and primates), published in the Journal of Cerebral Blood Flow & Metabolism in December 2014, found that in those who had suffered an ischemic stroke (temporary or permanent), the amount of the brain injured as a result was reduced in those subjects that had used cannabinoid therapies as opposed to those that had not.

Cannabis Treating Aneurysms

Marijuana Can Be an Effective Treatment for a Stroke

Conclusion: Cannabinoids effectively limit cell damage and provide patients with neuroprotective effects following a stroke.

Cannabinoids in the Treatment of Cerebral Aneurysm

Conclusion: Neuroprotective effects of cannabinoids could provide the basis for potential therapeutic uses of cannabinoids and/or endocannabinoids in stroke.

Cannabidiol enhances morphine antinociception, diminishes NMDA-mediated seizures and reduces stroke damage via the sigma 1 receptor

in vivo administration of CBD or BD1063 enhanced morphine-evoked supraspinal antinociception, alleviated NMDA-induced convulsive syndrome, and reduced the infarct size caused by permanent unilateral middle cerebral artery occlusion.

A cannabinoid receptor 2 agonist reduces blood-brain barrier damage via induction of MKP-1 after intracerebral hemorrhage in rats

Conclusions: CB2R agonist alleviated neuroinflammation and protected blood-brain barrier permeability in a rat ICH model. Further molecular mechanisms revealed which is probably mediated by enhancing the expression of MKP-1, then inhibited MAPKs signal transduction.

Emerging therapeutic targets associated with the immune system in patients with intracerebral haemorrhage

Various pathobiological processes contribute to secondary brain injury closely interact with the immune system. Hence, we summarize the immune response to ICH and recent progress in treatments targeting the immune system in this review. The emerging therapeutic strategies that target the immune system after ICH are a particular focus and have been summarized.


Cannabinoids and Epilepsy

Cannabis has been used for centuries to treat seizures. Characterized by recurrent seizures, epilepsy encompasses multiple disorders caused by varied etiologies, including congenital syndromes, stroke, infection, and traumatic brain injury. Many patients with epilepsy also have sensorimotor, cognitive, psychological, psychiatric, and social impairments, as well as impaired quality of life and an increased risk of premature death. Epilepsy most commonly affects children, the elderly, and individuals with low socioeconomic status.

Produced in an activity-dependent manner, endocannabinoids travel to the presynaptic cell and bind to cannabinoid receptor 1 (CB1Rs). CB1Rs are guanine nucleotide-binding protein-coupled receptors linked to pertussis-sensitive Gi/o a subunits. Activation of the α subunit triggers dissociation of the ßγ complex, which reduces adenylate cyclase production of cyclic adenosine monophosphate, inhibits N- and P/Q-type voltage-gated calcium channels, stimulates A-type potassium channels, activates guanine nucleotide-binding protein-coupled inwardly-rectifying potassium channels, and inhibits the vesicular release machinery.

CB1Rs can also regulate the presynaptic release of multiple neuromodulators such as acetylcholine, dopamine, and norepinephrine.

CB1Rs are distributed primarily in axon terminals in the neocortex (especially cingulate, frontal, and parietal regions), hippocampus, amygdala, basal ganglia, thalamus, hypothalamus, nucleus accumbens, substantia nigra, ventral tegmental area, cerebellum, and brainstem.

For over a millennium, pre-clinical and clinical evidence have shown that cannabinoids such as CBD can be used to reduce seizures effectively, particularly in patients with treatment-resistant epilepsy.

Phytocannabinoids and epilepsy

Conclusion: Phytocannabinoids produce anticonvulsant reactions through the endocannabinoid system, with few adverse effects.

Analysis in conditional cannabinoid 1 receptor-knockout mice reveals neuronal subpopulation-specific effects on epileptogenesis in the kindling paradigm

Conclusion: The endocannabinoid system plays an active role in seizure termination but does not regulate epileptogenesis.


Cannabis Use and Cognition in Schizophrenia

Conclusion: Our own results confirm the overall impression from the literature review of better cognitive performance in the cannabis user group. A majority of the studies report better cognitive functioning in the cannabis-related schizophrenia and psychosis groups compared to non-drug groups.

A systematic review of the antiPsychotic properties of cannabidiol in humans.

Conclusion: The first small-scale clinical studies with CBD treatment of patients with psychotic symptoms further confirm the potential of CBD as an effective, safe and well-tolerated antiPsychotic compound

Cannabidiol enhances anandamide signaling and alleviates psychotic symptoms of schizophrenia

Conclusion: Experimental studies show that cannabidiol reduces psychosis-like effects of Δ9-tetrahydrocannabinol and synthetic analogs.

Decreased glial reactivity could be involved in the antiPsychotic-like effect of cannabidiol.

Conclusion: our data support the view that inhibition of microglial activation may improve schizophrenia symptoms.


A possible role for the endocannabinoid system in the neurobiology of depression

Conclusion: Although data available are sufficient to suggest a possible involvement of the endogenous cannabinoid system in the neurobiology of depression, additional studies should be performed in order to better elucidate the role of this system in the physiopathology of depression.

Antidepressant-like effects of Δ9-tetrahydrocannabinol and rimonabant in the olfactory bulbectomised rat model of depression.

Conclusion: These findings indicate antidepressant-like behavioural properties of both THC and rimonabant in OB rats although additional studies are required to clarify the relationship between the chronic effects of cannabinoids in other pre-clinical models and in human depression.

Antidepressant-like effects of cannabidiol in mice: possible involvement of 5-HT1A receptors.

Conclusion: CBD induces antidepressant-like effects comparable to those of imipramine. These effects of CBD were probably mediated by activation of 5-HT(1A) receptors.


Cannabinoid CB1 receptors in the dorsal hippocampus and prelimbic medial prefrontal cortex modulate anxiety-like behavior

Conclusion: Endocannabinoids (ECBs) such as anandamide (AEA) act by activating cannabinoid type 1 (CB1) or 2 (CB2) receptors. The anxiolytic effect of drugs that facilitate ECB effects is associated with increase in AEA levels in several encephalic areas, including the prefrontal cortex (PFC). We observed that drugs which interfere with ECB reuptake/metabolism in both the PL and in the dentate gyrus of the dHIP induced anxiolytic-like effect, in both the EPM and in the VCT via CB1 receptors, suggesting that CB1 signaling in these brain regions modulates defensive responses to both innate and learned threatening stimuli. This data further strengthens previous results indicating modulation of hippocampal and MPFC activity via CB1 by ECBs, which could be therapeutically targeted to treat anxiety disorders. Modulation of hippocampal and MPFC activity via CB1 by ECBs, which could be therapeutically targeted to treat anxiety disorders.

conditioned fear

2-AG promotes the expression of conditioned fear via cannabinoid receptor type 1 on GABAergic neurons

The cannabinoid receptor type 1 (CB1) antagonist SR141716 (3 mg/kg) caused an increase in conditioned freezing upon repeated tone presentation on three consecutive days. 2-AG fear-promoting effects depended on CB1 signaling in GABAergic neurons, while an involvement of glutamatergic neurons remained inconclusive due to the high freezing shown by vehicle-treated Glu-CB1-KO.

amyotrophic lateral sclerosis

Cannabis and amyotrophic lateral sclerosis

Conclusion: Based on the currently available scientific data, it is reasonable to think that cannabis might significantly slow the progression of ALS, potentially extending life expectancy and substantially reducing the overall burden of the disease.

Survey of cannabis use in patients with amyotrophic lateral sclerosis

Conclusion: Although the small number of people with ALS that reported using cannabis limits the interpretation of the survey findings, the results indicate that cannabis may be moderately effective at reducing symptoms of appetite loss, depression, pain, spasticity, and drooling.

multiple sclerosis

Multiple Sclerosis

Multiple sclerosis (MS) is a chronic central nervous system inflammatory disease of autoimmune etiology, mediated by activated T-cells with evolving evidence of a significant contribution from B cells and cells of the innate immune system.

Clinical aspects

Multiple sclerosis is a chronic, predominantly immune-mediated disease of the central nervous system, and one of the most common causes of neurological disability in young adults globally. Multiple sclerosis is increasing in incidence and prevalence globally, even in traditionally low-prevalence regions of the world. Classifying multiple sclerosis into distinct disease phenotypes can be challenging, and recent refinements have been proposed to clarify existing definitions. The prognosis of multiple sclerosis varies substantially across individual patients.

Epidemiology of Multiple Sclerosis

The epidemiology of multiple sclerosis (MS) includes a consideration of genetic and environmental factors. Comparative studies of different populations have revealed prevalence and incidence rates that vary with geography and ethnicity. With a prevalence ranging from 2 per 100,000 in Japan to greater than 100 per 100,000 in Northern Europe and North America, the burden of MS is similarly unevenly influenced by longevity and comorbid disorders.

There is evidence for the use of cannabinoids for symptomatic treatment of multiple sclerosis

Conclusion: There is evidence that nabiximols oromucosal spray may reduce subjective symptoms of spasticity and that dronabinol is effective against neuropathic pain in patients with MS.

Smoked cannabis for spasticity in multiple sclerosis

Conclusion: Smoked cannabis was superior to placebo in symptom and pain reduction in participants with treatment-resistant spasticity.

Cannabinoids inhibit neurodegeneration in models of multiple sclerosis

Conclusion: Cannabinoids inhibit neurodegeneration in models of multiple sclerosis. In addition to symptom management, cannabis may also slow the neurodegenerative processes that ultimately lead to chronic disability in multiple sclerosis

Activation of Cannabinoid CB2 receptors Reduces Hyperalgesia in an Experimental Autoimmune Encephalomyelitis Mouse Model of Multiple Sclerosis

Conclusion: Our results suggest that JWH-133 acts at CB2 receptors, most likely within the dorsal horn of the spinal cord, to suppress the hypersensitivity associated with experimental autoimmune encephalomyelitis.


Cannabidiol for the treatment of psychosis in Parkinson' disease

The psychotic symptoms evaluated by the Brief Psychiatric Rating Scale and the Parkinson Psychosis Questionnaire showed a significant decrease under CBD treatment. CBD did not worsen the motor function and decreased the total scores of the Unified Parkinson' Disease Rating Scale. No adverse reaction was observed during the treatment. These preliminary data suggest that CBD may be effective, safe and well tolerated for the treatment of the psychosis in PD.

Parkinson' Disease and Parkinsonism

Parkinson' disease is a progressive neurodegenerative disease characterized by tremor and bradykinesia and is a common neurologic ailment. Male sex and advancing age are independent risk factors and, as the population ages, is taking an increasing toll on productivity and medical resources. There are a number of other extrapyramidal conditions that can make the diagnosis challenging.

Effects of cannabidiol in the treatment of patients with Parkinson' disease: an exploratory double-blind trial

Conclusion: Parkinson' disease (PD) has a progressive course and is characterized by the degeneration of dopaminergic neurons. Although no neuroprotective treatments for PD have been found to date, the endocannabinoid system has emerged as a promising target. Our findings point to a possible effect of CBD in improving quality of life measures in PD patients with no psychiatric comorbidities

Cannabis (medical marijuana) treatment for motor and non-motor symptoms of Parkinson disease

Conclusion: Significant improvement of sleep and pain scores. No significant adverse reaction of the drug were observed. The study suggests that cannabis might have a place in the therapeutic armamentarium of PD.

Symptom-relieving and neuroprotective effects of the phytocannabinoid Δ9-THCV

Conclusion: Given its antioxidant properties and its ability to activate CB2 but to block CB1 receptors, Δ9-THCV has a promising pharmacological profile for delaying disease progression in PD and also for ameliorating parkinsonian symptoms.

Cannabinoids provide neuroprotection against 6-hydroxydopamine toxicity

Conclusion: Our results support the view of a potential neuroprotective action of cannabinoids against the in vivo and in vitro toxicity of 6-hydroxydopamine, which might be relevant for PD. Our data indicated that these neuroprotective effects might be due, among others, to the antioxidant properties of certain plant-derived cannabinoids, or exerted through the capability of cannabinoid agonists to modulate glial function, or produced by a combination of both mechanisms.

Δ9-tetrahydrocannabinol (THC) exerts a direct neuroprotective effect in a human cell culture model of Parkinson' disease.

Conclusion: We have demonstrated up-regulation of the CB1 receptor in direct response to neuronal injury in a human PD cell culture model, and a direct neuronal protective effect of Δ9-THC that may be mediated through PPAR? activation.

Promising cannabinoid-based therapies for Parkinson' disease

Parkinson' disease (PD) is a slow insidious neurological disorder characterized by a loss of dopaminergic neurons in the midbrain. The elements of the endocannabinoid system are highly expressed in the neural circuit of basal ganglia wherein they bidirectionally interact with dopaminergic, glutamatergic, and GABAergic signaling systems. Additional benefits provided by cannabinoid related compounds including CE-178253, oleoylethanolamide, nabilone and HU-210 have been reported to possess efficacy against bradykinesia and levodopa-induced dyskinesia in PD. The molecular identification of the CB1 and CB2 receptors, the ion channel TRPV1, with their respective endogenous ligand systems has opened a whole arena of pharmacological effects elicited by each one of these specific receptor targets. CB1 and CB2 receptors belong to the superfamily of guanine nucleotide-binding protein-coupled receptors, which are coupled to inhibitory G proteins.

CB1 receptors are most highly expressed on axons and nerve terminals, but substantial functional evidence also confirms their expression on somata. Autoradiography investigations have convincingly reported that the basal ganglia encompass the highest levels of both mRNA expression and binding sites for the CB1 receptor. Including striatum, other three regions that receive striatal efferent outputs, such as the globus pallidus, entopeduncular nucleus, and substantia nigra pars reticulata (SNpr), contain high levels of CB1 receptor binding sites. CB1 receptors are positioned in striatonigral (direct striatal efferent pathway) and striatopallidal (indirect striatal efferent pathway) projection neurons, which use gamma-aminobutyric acid (GABA) as a neurotransmitter. Glutamic acid decarboxylase, prodynorphin, substance P, as well as D1 or D2 dopaminergic receptors are other markers co-expressed in these pathways. Immunohistochemical, immunoblot and autoradiographical studies have suggested the presence of CB1 receptor in substantia nigra, striatum and globus pallidus. CB1 receptor immunolabeling is also abundant in SNpr.

A second cannabinoid receptor was discovered in a human promyelocytic cDNA library within a few years following discovery of the CB1 receptor. Based on its homology to the CB1 receptor and similar ligand binding profile, this receptor was named the CB2 receptor. CB2 receptors are primarily expressed on immune cells.

Prolific expression of CB2 receptors is found in β lymphocytes, large granular lymphocytes, monocytes, neutrophils, cytotoxic T lymphocytes, and Th lymphocytes.

Some reports have also stated the importance of vanilloid TRPV1 receptors in the basal ganglia and their ability to interact with ECBs. TRPV1 receptors have been studied for their role as molecular integrators of nociceptive stimuli present abundantly on sensory neurons. Apart from sensory neurons, TRPV1 receptors are also found in the basal ganglia circuitry co-localized with tyrosine hydroxylase, indicating that they are located in dopaminergic neurons of the nigrostriatal pathway.

The orphan guanine nucleotide-binding protein-coupled receptor 55 (GPR55) has been discovered as another possible cannabinoid receptor.

In comparison to CB receptors, GPR55 is coupled to Gq, Gα12, and Gα13 proteins.

Two sets of neuronal circuits exist for striatal MSNs that connect to the output nuclei of the basal ganglia. One is a direct circuit (direct pathway) or via a sequence of connections that include the STN and the external segment of the globus pallidus (GPe) (indirect pathway). The output nuclei [SNpr and the internal segment of the globus pallidus (GPi)] connect to the thalamus, which further has efferent extensions that form the cortico-basal ganglia-thalamo-cortical loop. The physiological effect of dopamine originating from the SNpc on MSNs is intricate and not fully revealed. In fact, the intensity of membrane depolarization on the dopamine receptor dictates the type of effect produced. D1 dopamine receptors are positively coupled to adenylyl cyclase; hence, their activation increases the cytosolic cAMP level and subsequently elicits numerous downstream effects including an increase in NMDA receptor-mediated currents. In contrast, D2 dopamine receptors are negatively coupled to adenylyl cyclase and their activation decreases neuronal excitability and neuronal feedback to glutamatergic inputs.

Activation of D1/D2 heteromers are demonstrated to mediate mechanisms like, increased intracellular Ca2+ levels, activation of calcium/calmodulin-dependent protein kinase II (CaMKII) and release of brain-derived neurotrophic factor (BDNF).


Neuroinflammation in Alzheimer' disease

Several attempts have been made to treat Alzheimer' disease (AD) using anti-amyloid strategies with disappointing results. It is clear that the "amyloid cascade hypothesis" alone cannot fully explain the neuronal damage in AD, as evidenced both by autopsy and imaging studies.

Neuroinflammation plays a significant role in neurodegenerative diseases, whereas the debate is ongoing about its precise role, whether it is protective or harmful. In this review, we focus on the potential mechanism of glial activation and how local and systemic factors influence disease progression. We focus on neuroinflammation in AD, especially in the earliest stages, a vicious cycle of glial priming, release of pro-inflammatory factors, and neuronal damage. We review the evidence from imaging studies, regarding the temporal relationship between amyloid deposition and neuroinflammation, the influence of systemic inflammation on glial activation, both in acute and chronic stimulation and the relevance of inflammation as a diagnostic and therapeutic target.

The potential therapeutic effects of THC on Alzheimer' disease

Conclusion: These sets of data strongly suggest that THC could be a potential therapeutic treatment option for Alzheimer' disease through multiple functions and pathways.

Neuroprotection Mediated by Blockade of Microglial Activation

Conclusion: Alzheimer' disease (AD) is characterized by enhanced ß-amyloid peptide (ßA) deposition along with glial activation in senile plaques, selective neuronal loss, and cognitive deficits. Cannabinoids are neuroprotective agents against excitotoxicity in vitro and acute brain damage in vivo. Recent studies on therapeutic strategies for neurodegenerative diseases such as Parkinson' disease and AD have focused on the neuroprotective properties (e.g., slowing the ongoing neurodegeneration) rather than just on palliating symptoms of the diseases (Dawson and Dawson, 2002). Because cannabinoids combine both anti-inflammatory and neuroprotective actions, our findings may set the basis for the use of these compounds as a therapeutic approach for AD.

A Molecular Link Between the Active Component of Marijuana and Alzheimer' Disease Pathology

Conclusion: Alzheimer' disease is the leading cause of dementia among the elderly, and with the ever-increasing size of this population, cases of Alzheimer' disease are expected to triple over the next 50 years. AChE inhibitors such as THC and its analogues may provide an improved therapeutic for Alzheimer' disease, augmenting acetylcholine levels by preventing neurotransmitter degradation and reducing Aß amalgamation, thereby simultaneously treating both the symptoms and progression of Alzheimer' disease.

Prolonged oral cannabinoid administration prevents neuroinflammation, lowers ß-amyloid levels and improves cognitive performance

Conclusion: Alzheimer' disease (AD) brain shows an ongoing inflammatory condition and non-steroidal anti-inflammatories diminish the risk of suffering the neurologic disease. Cannabinoids are neuroprotective and anti-inflammatory agents with therapeutic potential. We have shown that chronically administered cannabinoid showed marked beneficial effects concomitant with inflammation reduction and increased Aß clearance.


Cannabinoids reduce symptoms of Tourette's syndrome

Conclusion: Currently, the treatment of Tourette's syndrome (TS) is unsatisfactory. A single-dose, cross-over study in 12 patients, as well as a 6-week, randomised trial in 24 patients, demonstrated that Δ9-tetrahydrocannabinol (THC), the most psychoactive ingredient of cannabis, reduces tics in TS patients. No serious adverse reaction occurred and no impairment on neuropsychological performance was observed.

unique library index

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