I'm not recommending this. Just sharing something different.
Velvet Antler Methanol Extracts Ameliorate Parkinson's Disease by Inhibiting Oxidative Stress and Neuroinflammation: From C. elegans to Mice 2021 ncbi.nlm.nih.gov/labs/pmc/a...
"In all, this study dissected the pharmacology of MEs of velvet antler in PD. The C. elegans PD model studies show that MEs inhibit α-synuclein aggregation and protect DAergic neurons from degeneration. In vitro microglia cellular data indicate that MEs suppressed the LPS-induced MAPK and NF-κB activation, therefore inhibiting ROS and proinflammatory factors as well as the activation of microglia and protecting DAergic neurons from the microglia-mediated neurotoxicity. In vivo MPTP-induced PD mouse investigations demonstrate that MEs prevent MPTP-induced neuron loss in the substantia nigra and improve parkinsonism in MPTP-treated mice by increasing the expression level of TH and downregulating α-synuclein protein expression. Since MEs of velvet antler have no apparent toxicology, MEs would have good translational potential for preventing and treating PD."
If you Google "Velvet Antler Methanol Extract" you get a lot of products.
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Bolt_Upright
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In the worm study the larval worms were first exposed to toxin and immediately transferred to treatment medium. So it is not clear to me what stage of development of Parkinson's they received treatment.
For the mouse study, on the other hand:
" MPTP plus ME-treated group (intraperitoneal injection of 30 mg/kg MPTP and 30 mg/kg MEs for 5 days"
ME extract being the methanol extract of the velvet antler. So they are treated with toxin and therapy at the same time. As previously discussed, even a simple antioxidant can be effective at preventing toxic damage at this point. This is not valid evidence of effectiveness in Parkinson's.
Deer antler velvet contains IGF-1, a prohormone/steroid. Athlete's use it for doping, we could learn a lot from them
Insulin‐Like Growth Factor‐1 (IGF‐1) is neuroprotective. Glycine‐Proline‐Glutamate (GPE) is naturally cleaved from the IGF‐1 N‐terminal and is also neuroprotective, thus providing a potential novel strategy of drug discovery for management of neurological disorders.
Neuroprotection by GPE and its analogue may be involved in modulation of inflammation, promotion of astrocytosis, inhibition of apoptosis, and in vascular remodeling.
Glycine-Proline-Glutamate (GPE), was, until the late 1980s, generally believed to be a nonbioactive byproduct of IGF-1 metabolism. Synthetic GPE stimulated both dopamine and acetylcholine release in brain slice culture without interacting with IGF-1 receptors. GPE showed partial displacement by an N-methyl d-aspartate (NMDA) receptor antagonist in cell culture. Saura et al. showed that GPE dose-dependently protected hippocampal neurons from NMDA-induced neuronal toxicity.
With glycine and glutamate at opposite ends of the molecule, GPE appears to have the perfect stereochemistry to activate NMDA receptors by binding to both the glutamate and glycine binding sites of the receptor. Both antagonistic and agonistic effects of GPE have been demonstrated.
Inhibiting caspase-3-activated and noncaspase-3-activated apoptotic pathways may be involved in the neuroprotection by GPE, by antagonistic activity of GPE and IGF-1, acting as a prohormone of GPE on NMDA receptors. Caspase-3 immunostaining have been widely used as markers of neurons that undergo apoptosis, in which neurons are committed to die via a progressive process.
NMDA receptors play a critical role in various aspects of CNS function. Hence, it is important to identify mechanisms that regulate NMDA receptor activity.
Insulin rapidly potentiates NMDA receptor activity. The same receptors for excitatory amino acids (EAA) that mediate direct neuronal depolarization can also be responsible for neuronal injury. Prolonged stimulation of EAA receptors of either the N-methyl-d-aspartate (NMDA) or non-NMDA types eventually results in the death of most central neurons.
N-Methyl-d-aspartate (NMDA) receptors belong to the family of ionotropic glutamate receptors, which mediate most excitatory synaptic transmission in mammalian brains. Calcium permeation triggered by activation of NMDA receptors is the pivotal event for initiation of neuronal plasticity.
Neurodegenerative illnesses may be at least partially produced by excessive activation of NMDA receptors.
To the extent that the pathophysiology can be explained by this mechanism, it may be amenable to rational therapies now under development.
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