3. Umbruch 4.4..2005 - Online Pot

Cannabinoids in neurodegeneration and neuroprotection 89
Table 1. Neuroprotective effects of cannabinoid-related compounds in acute or chronic neurodegenerative
disorders
Disease Therapeutic applications References
Acute neurodegeneration
Reduction of infart size (and associated edema) and
neurological deficits by cannabinoid agonists in
rodents with global or focal cerebral ischemia, or
subjected to closed head injury.
[4–6, 15, 30, 109]
Increase of cell survival by several cannabinoid [6, 28–30, 55,
agonists in cultured neurons (from different regions)
subjected to hypoxia and/or glucose deprivation, or
exposed to excitotoxins.
56, 88, 111]
Neuroprotection provided by direct or indirect
cannabinoid agonists in rodents subjected to
excitotoxic stimuli. Greater brain injury in CB1 receptor-deficient mice subjected to ischemia.
Chronic neurodegeneration
[9, 10, 13, 50, 113]
Huntington’s Reduction of striatal injury by ∆ 9 -THC in a non- [65]
disease (HD) apoptotic rat model (lesions with 3-nitropropionic
acid).
CB2 receptor-mediated neuroprotection by cannabinoids
in a rat model of striatal injury that progresses
through apoptotic death (local applications of
malonate); CBD exerted poor neuroprotective action
in this model, whereas SR-141716 increased striatal
damage.
[19, 32]
Parkinson’s Reduction of dopaminergic injury in the 6-hydroxy- [64]
disease (PD) dopamine rat model by ∆ 9 -THC and CBD.
Increased cell survival in vitro exerted by HU-210
through enhancing glial influences to neurons.
[64]
Alzheimer’s Prevention of β-amyloid toxicity in vitro by AEA, [176, 177]
disease (AD) noladin-ether or CBD.
Multiple Reduction of motor deterioration in EAE rats by [186–188]
sclerosis (MS) plant-derived cannabinoids or uptake inhibitors.
Improvement of motor function, reduction of activated
microglia, and promotion of remyelination by several
cannabinoid agonists in a Theiler’s murine encephalomyelitis
model.
[189, 190]
CB1 receptor-deficient mice were more vulnerable to
inflammatory and excitotoxic insults following immune
attack in EAE.
[184]
Amyotrophic Delayed motor impairment and increased survival [192]
lateral sclerosis after ∆ 9 -THC administration in a genetic mouse model
(ALS) of ALS.
WIN-55,212-2 was protective in vitro and also in an in vivo model of ischemic
damage. Anandamide and 2-AG have been also found to protect rat cortical
neurons from in vitro ischemia [111]. In another studies using in vivo models,