LeafyCeuticals presents the discussion of Alzheimer's disease because a recent scientific study indicated that the CBDA cannabinoid can inhibit and even reverse some of the symptoms of Alzheimer's. Notably, hints that cannabis could slow Alzheimer’s circulated for years. The CBDA in the study naturally occurs in the Leafyceuticals StopsNausea product.
Alzheimer's disease slowly but steadily impairs brain functions, usually with a fatal outcome. Alzheimer's disease (AD) likely refers to a variety of forms of dementia that share some common features. The precise cause of AD remains unclear, but examination of brain tissues shows that patients suffer from a build-up of Amyloid-beta. The amyloid-beta molecules degrade brain cell functioning to the point of cell death. As these brain cells die, eventually the brain shrinks and physical management of the body ceases.
Tau-proteins within the axons of the neurons also develop and disrupt the brain cells’ internal functioning. The tau-protein hypothesis suggests that proteins used to construct microtubules become chemically modified (called hyperphosphorylation). The modified proteins may cause normal proteins to be degraded and dissolve the microtubules. The microtubules that provide structure and a metabolic framework to the neuron axon, converted into tau tangles ultimately cause the cell’s death.
Amyloid beta develops when the normally occurring Amyloid beta Precursor Protein (APP) undergoes an abnormal breakdown. Research has not determined the function of the APP glycoprotein which is normally embedded in the neuronal cell membrane. Some change in brain metabolism causes the APP to be cleaved by two enzymes and to generate peptides 39-43 amino acids in length. The peptides accumulate and coalesce to form beta-amyloid plaques. The change in conditions that give rise to making Amyloid beta remain unclear.
The amyloid hypothesis suggests that the accumulation and aggregation of beta-amyloid peptides disrupt the cell's calcium ion balance resulting in cell death. Research suggests that clumping of Amyloid beta peptides generates reactive chemicals. These chemicals destroy the proteins involved in ion-transport metabolism, and result in calcium influx and membrane depolarization.
Both amyloid beta and tau proteins may proliferate as misfolded ‘seeds’ cause misfolding in newly generated molecules, and further clumping.
The death of brain cells generates inflammation and may trigger a cycle where still other cells lose viability. Epidemiology has identified several genes that signify increased risk of AD. Some of these genes code for factors that affect normal clearance of misfolded proteins or for inflammatory reactions. Research suggests that systemic inflammation and obesity interfere with the immune system and allow or cause Alzheimer’s disease progression.
The allele named Apo-E4 increases risk for Alzheimer's but many other risk factors have been identified including lifestyle and other physical conditions. The use of cholesterol controlling statins seems to confer a lower risk of AD.
AD can cause subtle or apparent losses to motor control, muscle tone and balance. However, the symptoms that signal onset typically involve losses of memory, concentration and problem solving. These may progress to confusion, personality changes and cognition. AD is the most common form of dementia.
The way Alzheimer's incapacitates people often takes a heavy toll on the patient’s caregivers as well as friends and family who steadily lose contact with the person they knew. The lengthy duration inflicts heavy financial burdens as well. The diagnosis of Alzheimer's may require specialists to rule out other conditions and only yields 90% accuracy. Although Alzheimer's can begin before 40, most cases begin after 65. More than 6 million people suffer from Alzheimer's in the US.
The FDA approved Memantine for treatment of Alzheimer’s. Memantine inhibits the N-methyl-D-aspartate (NMDA) calcium receptor. The inhibition of the NMDA receptor lowers the intracellular calcium levels. CBD may be similar in action to Memantine in that CBD acts as a σ1R antagonist to the NMDA receptor. It is likely that CBDA acts like CBD and Memantine. Perhaps CBDA has an outsized effect on the NMDA receptor similar to the way that CBDA is hundreds of times more effective than CBD in quelling nausea. CBDA (and THCA) also slow calcium influx when they inhibit T-type calcium channels. Lastly, CBDA works as a more potent anti-inflammatory than CBD.
As an aside, the big picture is this. While marijuana had its roots in racism, the criminalization of marijuana effectively shut down all research into its medical benefits. By stopping all medical research on cannabinoids, this foreclosed discovery of its effects against cancer, epilepsy, pain management and now Alzheimer’s Disease. Imagine a world where people use herbal cannabis to prevent these and other diseases! Millions have suffered the worst agonies in order to enable ‘certain people’ to express their racism. A better world awaits when society resists these ugly impulses.
Apolipoprotein E (Apo-E) is a protein involved in the metabolism of fats in the body of mammals. A subtype is implicated in the Alzheimer's disease and cardiovascular diseases.[5] It is encoded in humans by the gene APOE.
Apo-E belongs to a family of fat-binding proteins called apolipoproteins. In the circulation, it is present as part of several classes of lipoprotein particles, including chylomicron remnants, VLDL, IDL, and some HDL.[6] APOE interacts significantly with the low-density lipoprotein receptor (LDLR), which is essential for the normal processing (catabolism) of triglyceride-rich lipoproteins.[7] In peripheral tissues, APOE is primarily produced by the liver and macrophages, and mediates cholesterol metabolism. In the central nervous system, Apo-E is mainly produced by astrocytes and transports cholesterol to neurons[8] via APOE receptors, which are members of the low density lipoprotein receptor gene family.[9] Apo-E is the principal cholesterol carrier in the brain.[10] Apo-E is required for cholesterol transportation from astrocytes to neurons.[8] APOE qualifies as a checkpoint inhibitor of the classical complement pathway by complex formation with activated C1q.[
Amyloid beta (Aβ or Abeta) denotes peptides of 36–43 amino acids that are the main component of the amyloid plaques found in the brains of people with Alzheimer's disease.[2] The peptides derive from the amyloid-beta precursor protein (APP), which is cleaved by beta secretase and gamma secretase to yield Aβ in a cholesterol-dependent process and substrate presentation.[3] Aβ molecules can aggregate to form flexible soluble oligomers which may exist in several forms. It is now believed that certain misfolded oligomers (known as "seeds") can induce other Aβ molecules to also take the misfolded oligomeric form, leading to a chain reaction akin to a prion infection. The oligomers are toxic to nerve cells.[4] The other protein implicated in Alzheimer's disease, tau protein, also forms such prion-like misfolded oligomers, and there is some evidence that misfolded Aβ can induce tau to misfold.[5][6]
Several investigations reported that medicinal plants are utilized in the Alzheimer's disease treatment which includes Centella asiatica, Ginkgo biloba, Withania somnifera, Bacopa monnieri, Salvia officinalis, Melissa officinalis, Tinospora cordifolia, Glycyrrhiza glabra etc.
Herbs that can help those living with Dementia
Turmeric. Alzheimer's and dementia occur a significant amount less in India than England – which is thought to be due to turmeric and its primary component; curcumin, and their antioxidant benefits.
Holy Basil.
Ginkgo Biloba.
Ginseng
Cannabidiol (CBD) has numerous pharmacological targets that initiate anti-inflammatory, antioxidative, and antiepileptic properties. These neuroprotective benefits have generated interest in CBD's therapeutic potential against the secondary injury cascade from traumatic brain injury (TBI).
NMDA (short for N-methyl-D-aspartate) receptor antagonists are a class of drugs that may help treat Alzheimer's disease, which causes memory loss, brain damage, and, eventually, death. There's no cure for Alzheimer's, but some drugs may slow it down.
If you have Alzheimer's disease, your cells can make too much glutamate. When that happens, the nerve cells get too much calcium, and that can speed up damage to them. NMDA receptor antagonists make it harder for glutamate to "dock" -- but they still let important signals flow between cells. Scientists are studying how they can be used against Alzheimer's.
The FDA approved Memantine, an antagonist of the N-methyl-D-aspartate (NMDA) calcium receptor, as a drug for treating AD [50]. Memantine lowers intracellular calcium concentrations by inhibiting the NMDA calcium receptor [51]. A decrease in calcium concentration following Memantine treatment results in neuroprotection, learning, and cognitive function, exhibits inhibitory effects on Aβ and p-tau production and activates the BDNF/CREB signaling pathway. ///