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huntington disease/cannabis
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Loss of striatal type 1 cannabinoid receptors is a key pathogenic factor in Huntington's disease.
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Endocannabinoids act as neuromodulatory and neuroprotective cues by engaging type 1 cannabinoid receptors. These receptors are highly abundant in the basal ganglia and play a pivotal role in the control of motor behaviour. An early downregulation of type 1 cannabinoid receptors has been documented
Delayed onset of Huntington's disease in mice in an enriched environment correlates with delayed loss of cannabinoid CB1 receptors.
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Huntington's disease (HD) is a late onset progressive genetic disorder characterised by motor dysfunction, personality changes, dementia and premature death. The disease is caused by an unstable expanded trinucleotide (CAG) repeat encoding a polyglutamine stretch in the IT15 gene for huntingtin, a
Effects of cannabinoids in the rat model of Huntington's disease generated by an intrastriatal injection of malonate.
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Cannabinoids could provide neuroprotection in neurodegenerative disorders. In this study, we examined whether a treatment with Delta9-tetrahydrocannabinol, a non-selective cannabinoid receptor agonist, or with SR141716, a selective antagonist for the cannabinoid CB(1) receptor subtype, could affect
Chronic cannabinoid receptor stimulation selectively prevents motor impairments in a mouse model of Huntington's disease.
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Huntington's disease (HD) is a devastating neurodegenerative disease characterized by a progressive decline in motor abilities, as well as in cognitive and social behaviors. Most of these behavioral deficits are recapitulated in the R6/1 transgenic mouse, which can therefore be used as an
Cannabinoids: novel medicines for the treatment of Huntington's disease.
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Cannabinoid pharmacology has experienced a notable increase in the last 3 decades which is allowing the development of novel cannabinoid-based medicines for the treatment of different human pathologies, for example, Cesamet® (nabilone) or Marinol® (synthetic Δ9-tetrahydrocannabinol for oral
Cannabinoids for Treatment of Dystonia in Huntington's Disease.
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BACKGROUND
Motor symptoms in Huntington's disease (HD) are heterogeneous with dystonia being described as a symptom with a very high prevalence not only in juvenile cases.
OBJECTIVE
Treatment options for dystonia are limited. Cannabinoids have been described as a potential treatment for patients
Cannabinoids increase type 1 cannabinoid receptor expression in a cell culture model of striatal neurons: implications for Huntington's disease.
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The type 1 cannabinoid receptor (CB1) is a G protein-coupled receptor that is expressed at high levels in the striatum. Activation of CB1 increases expression of neuronal trophic factors and inhibits neurotransmitter release from GABA-ergic striatal neurons. CB1 mRNA levels can be elevated by
Abnormal sensitivity to cannabinoid receptor stimulation might contribute to altered gamma-aminobutyric acid transmission in the striatum of R6/2 Huntington's disease mice.
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BACKGROUND
One of the earliest neurochemical alterations observed in both Huntington's disease (HD) patients and HD animal models is the dysregulation of the endocannabinoid system, an alteration that precedes the development of identifiable striatal neuropathology. How this alteration impacts
Downregulation of cannabinoid receptor 1 from neuropeptide Y interneurons in the basal ganglia of patients with Huntington's disease and mouse models.
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Cannabinoid receptor 1 (CB(1) receptor) controls several neuronal functions, including neurotransmitter release, synaptic plasticity, gene expression and neuronal viability. Downregulation of CB(1) expression in the basal ganglia of patients with Huntington's disease (HD) and animal models
Structure, expression and regulation of the cannabinoid receptor gene (CB1) in Huntington's disease transgenic mice.
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Loss of cannabinoid receptors (CB1) occurs prior to neurodegeneration in Huntington's disease (HD). The levels and distribution of CB1 RNA were equivalent in 3-week-old mice regardless of genotype demonstrating that the specific factors and appropriate chromatin structure that lead to the
A novel population of progenitor cells expressing cannabinoid receptors in the subependymal layer of the adult normal and Huntington's disease human brain.
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Progenitor cells in the adult human brain subependymal layer are capable of producing new neurons and glial cells that may be useful as a source of cells for endogenous cell replacement for regions of the brain that undergo degeneration due to a neurodegenerative disease such as Huntington's
Cannabinoid receptor CB2 is expressed on vascular cells, but not astroglial cells in the post-mortem human Huntington's disease brain.
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Huntington's disease (HD) is an inherited neurological disease with motor, cognitive and psychiatric symptoms. Characterised by neuronal degeneration, HD pathology is initially apparent in the striatum and cortex. Considerable research has recently suggested that the neurological immune response
Cannabinoid (CB(1)), GABA(A) and GABA(B) receptor subunit changes in the globus pallidus in Huntington's disease.
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Huntington's disease (HD) is a disease of the basal ganglia which results in a major loss of the striatal GABAergic medium spiny neurons containing enkephalin and substance P. These neurons project principally to the globus pallidus (GP) and substantia nigra pars reticulata (SNr). Both GABA(A) and
Selective vulnerability in Huntington's disease: preferential loss of cannabinoid receptors in lateral globus pallidus.
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Selective neuronal vulnerability is a key feature of the neuropathology of Huntington's disease. We used [3H]CP-55,940, a synthetic cannabinoid, to label cannabinoid receptors in tissue sections from individuals dying with Huntington's disease and from normal control subjects. The density of
Cannabinoid CB2 receptor agonists protect the striatum against malonate toxicity: relevance for Huntington's disease.
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Cannabinoid agonists might serve as neuroprotective agents in neurodegenerative disorders. Here, we examined this hypothesis in a rat model of Huntington's disease (HD) generated by intrastriatal injection of the mitochondrial complex II inhibitor malonate. Our results showed that only compounds
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