Below, the reader is given information about the components of Alz-Halt HG. Since this was the initial Alz-Halt product, it could be referred to simply as Alz-Halt.
Leafyceuticals makes supplements compounded to oppose the symptoms of Alzheimer’s Disease (AD). The information below describes the action of hemp components on Alzheimer’s processes. People over 40 begin to display the same changes in their brains as Alzheimer’s victims. Thus, the Alz-Halt HG remedy should help anyone to preserve their memory, clarity, and cognitive functions. It may also help others who may have post-Covid brain fog or other mental losses.
“AlzHalt HG” contains Cannabidiol or CBD. Hemp contains both CBD and its acid precursor, CBDA. When heating Cannabidiolic Acid (CBDA), carbon dioxide (CO2) is released, and the molecule transforms into CBD. AlzHalt HG also contains Ginger Root Extract, which similarly shows action that opposes the progression of Alzheimer’s Disease.
The hemp comes from Oregon and the laboratory analysis may be viewed by using a phone camera to register the label’s QR code. Hemp contains more than 100 cannabinoids including CBD and CBDA. Hemp contains more CBDA than any other cannabinoid. Hemp has less than 0.3% THC, so one doesn’t become intoxicated by consuming hemp.
In Alzheimer’s Disease, improper processing of amyloid precursor protein (APP) produces Amyloid β-protein (Aβ) which then accumulates into inflammatory plaque. Inflammation from Aβ plaque leads to neuronal loss in several brain regions. P-tau refers to misfolded proteins that form tau tangles inside neurons. P-tau also causes inflammation and eventually kills the cell.
Under normal circumstances, the immune system elevates reactive oxygenated species (ROS) to neutralize pathogens. The white blood cells, macrophages and neutrophils, can trigger a “respiratory burst” when acting against pathogens. However, these oxygenated molecules can upset the balance of calcium and trigger production of amyloid plaque and tau-tangles.
A recent study found that CBDA and THCA lowered Aβ and p-tau levels. Aβ and p-tau are associated with a high intracellular calcium level. CBDA treatment restored normal calcium levels along with reducing inflammation. For demented patients, the high calcium level inhibits signal transmission and thus memory creation in impaired.1
CBDA also stops or moderates headaches (hyperalgesia) and nausea. CBD can reduce seizures, anxiety, and depression.1
How does CBD work?
CBDA and CBD have several modes of action. One mode is to control phosphorylation by decreasing ATP production. CBDA and CBD activate receptors on the surface of mitochondria, the ATP generators. Receptor activation reduces the activity of the enzyme adenyl cyclase that produces ATP.2
Cannabinoids activate receptors on the surface of cell nuclei called PPARϒ. Triggering these nuclear receptors directly activates various genes. In this case, CBA (and CBDA) prevent the production of the Aβ proteins that form plaque.3 In addition to reducing inflammation, PPARϒ regulates fat cell development and boosts insulin sensitivity.4
In one study, “…object recognition deficits and delayed spatial learning… were reversed by CBD treatment.”5 Another study found “CBD also stimulated neurogenesis and promoted dendritic restructuring…”6
While Alz-Halt is intended to inhibit Alzheimer’s Disease (AD) processes, research shows that the anti-anxiety and anti-depression effects of CBD have utility in addressing the agitation sometimes seen with AD patients.7 Depression of AD patients has importance because the condition often triggers institutionalization which, in turn, makes the AD worse.8
Glial cells, microglia and astrocytes defend the brain. Microglia cells release reactive oxygen species and the anti-inflammatory cytokines, TGF-β1 and IL-10. Cannabinoids like CBDA and CBD activate the nuclear receptor, PPARϒ with the downstream effect of inhibiting NF-κB pathway and reducing inflammatory molecules. Studies suggest that cannabinoids reduce the level of Acetylcholinesterase (AChE). Both AChE and the NF-κB become elevated in AD patients.9
In AD brains, Aβ polymers activate microglia and astrocytes. This leads to an excessive release of proinflammatory agents, causing synaptic damage and memory impairment. CBD suppresses this glial activation and reduces proinflammatory cytokine levels
CBD may act to induce synapse repair. CBD significantly reduced mRNA levels of inflammatory agents (such as TNF-α and MCP-1) and thus reduced the cytokine levels. (TNF-α=Tumor Necrosis Factor, MCP-1= Monocyte chemoattractant protein-1). In vivo experiments documented CBD’s capacity to repair cognitive deficits and rejuvenate mental capabilities impaired by amyloid plaque.9
Research also found that CBD suppressed the phosphorylation of tau protein in Aβ-stimulated neurons. The CBD-induced suppression was associated with a reduction of the enzyme p-GSK3- β (phosphorylated glycogen synthase kinase 3-β). In AD patients, Tau proteins tangle inside the cells, eventually killing the cell. CBD appears to prevent this process.
One model of Alzheimer’s suggests that the condition arises from an imbalance in the forms of glutathione. This imbalance contributes to cognitive impairment.10 CBD reduced extracellular glutamate levels in the hippocampus of mice with AD.14
Alz-Halt HG has the advantage of providing CBDA as well as CBD. One study found “Cannabinoid acids bind and activate PPARϒ with higher potency than their decarboxylated products”11 Activation of PPARϒ may have beneficial effects on mitochondrial dysfunction, again a critical component of AD. PPARs (nuclear receptors) mediate transcription regulating lipid metabolism, energy balance, inflammation, cell growth, differentiation, and apoptosis(cell death).12
CBDA and CBD resemble the molecules made by the body to control the body. Science describes the originals as “Endocannabinoids”. This similarity means that cannabinoids affect multiple target receptors. CBDA also activates the serotonin receptor 5-HT1A and stops nausea as a result.13
Alz-Halt HP contains ginger which also inhibits the release of anti-inflammatory cytokines. “The cognitive enhancing effects of ginger might be partly explained by alteration of both the monoamine and the cholinergic systems in various brain areas.”15 Ginger also has antimicrobial, anti-inflammatory, antioxidant, anticancer and anti-allergy actions.9
SUMMARY
People over 40 begin to display the same changes in their brains as Alzheimer’s Disease (AD) victims. We formulated the Alz-Halt capsules to oppose the shifts in brain chemistry that cause AD. These cannabinoids restore neuronal vitality including developing new dendritic connections. These capsules should help anyone preserve their memory, clarity, and cognitive functions.
If one has other inflammatory conditions, the Alz-Halt HG and/or Alz-Halt CP should be used. Inflammatory conditions include arthritis, pre-diabetes, being overweight, muscle soreness, alcohol use, and low energy. Alz-Halt HG will help with anxiety, depression, allergies, and Irritable Bowel Syndrome (IBS).
References
1. Kim, Juyong, et. al. The Cannabinoids, CBDA and THCA, Rescue Memory Deficits and Reduce Amyloid-Beta and Tau Pathology in an Alzheimer’s Disease-like Mouse Model. Int J Mol Sci. 2023 Apr; 24(7): 6827. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10095267/
2. Malheiro, Rui, Filipe, et. al., Cannabinoid-mediated targeting of mitochondria on the modulation of mitochondrial function and dynamics, Pharmacological Research 2023 Jan:187:106603. https://pubmed.ncbi.nlm.nih.gov/36516885/
3. Coles, Madilyn, et. al., Therapeutic properties of multi-cannabinoid treatment strategies for Alzheimer’s disease, Cells 2023, 12(23), 2672; https://www.mdpi.com/2073-4409/12/23/2672
4. Nachnani, Rahul, et. al., The Pharmacological Case for Cannabigerol, J Pharmacol Exp Ther. 2021 Feb;376(2):204-212. https://pubmed.ncbi.nlm.nih.gov/33168643/
5. Coles, Madilyn, et. al., Medium-Dose Chronic Cannabidiol Treatment Reverses Object Recognition Memory Deficits of APP Swe/PS1∆E0 Transgenic Female Mice, Pharmacology. 2020 Dec 4:11-587604, https://pubmed.ncbi.nlm.nih.gov/33424597/
6. Mori, Marco Aurelio, et. al., Cannabidiol reduces neuroinflammation and promotes neuroplasticity and functional recovery after brain ischemia, Prog Neuropsychopharmacology biol Psychiatry 2017, Apr 3:75, 94-105., https://pubmed.ncbi.nlm.nih.gov/27889412/
7. Hermush, Vered, et. al., Effects of rich cannabidiol oil on behavioral disturbances in patients with dementia: A placebo controlled randomized clinical trial, Front Med (Lausanne) 2022 Sep 6:9:951889. https://pubmed.ncbi.nlm.nih.gov/36148467/
8. Fonseca, Carla, et. al., Under the umbrella of depression and Alzheimer's disease physiopathology: Can cannabinoids be a dual-pleiotropic therapy? Ageing Res Rev, 2023 Sep:90:101998. https://pubmed.ncbi.nlm.nih.gov/37414155/
9. Chen, Long, et. al., Assessing Cannabidiol as a Therapeutic Agent for Preventing and Alleviating Alzheimer’s Disease Neurodegeneration. Cells 2023, 12(23), 2672. https://www.mdpi.com/2073-4409/12/23/2672
10. Bermejo-Bescos, Paloma, et. al., A Diet Containing Rutin Ameliorates Brain Intracellular Redox Homeostasis in a Mouse Model of Alzheimer's Disease, Int J Mol Sci. 2023 Mar 2;24(5):4863, https://pubmed.ncbi.nlm.nih.gov/36902309/
11. Nadal, Xavier, et. al., British J. of Pharmacology (2017) 174:4263-4276. Tetrahydrocannabinolic acid is a potent PPARϒ agonist with neuroprotective activity. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5731255
12. Lago-Fernandez, Ana, et. al., Relevance of Peroxisome Proliferator Activated Receptors in Multitarget Paradigm Associated with the Endocannabinoid System. Int J Mol Sci 2021 Jan 20;22(3):1001. https://pubmed.ncbi.nlm.nih.gov/33498245/
13. Rock, Erin M., et. al. Cannabinoid Regulation of Acute and Anticipatory Nausea. Cannabis and Cannabinoid Research Volume 1.1,2016. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5576606/
14. Rupprecht, Anne, et. al., The Combination of Δ9-Tetrahydrocannabinol and Cannabidiol Suppresses Mitochondrial Respiration of Human Glioblastoma Cells via Downregulation of Specific Respiratory Chain Proteins, Cancers (Basel). 2022 Jul; 14(13): 3129. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9265124
15. Schepici, Giovanni, et. al., Ginger, a Possible Candidate for the Treatment of Dementias? Molecules. 2021 Sep; 26(18): 5700. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8470323/
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