Amyloid beta: The alternate hypothesis — UT San …

Dendritic function of tau mediates amyloid-beta toxicity in Alzheimer's disease mouse models.

Beyond the Failed Beta Amyloid Hypothesis -- Alzheimer…

We cite the following abstract of an article, "Treating Alzheimer’sDisease by Inactivating Bioactive Amyloid-Beta Peptide" by Liu &Schubert to give our readers an idea of the amyloid-beta hypothesis:

Models of β-amyloid induced Tau-pathology: the long and "folded" road to understand the mechanism.

Amyloid Beta: The Alternate Hypothesis | BenthamScience


Steinbach Online, November 2017
Due to recent research, curcumin has been nicknamed the "master off-switch for inflammation." It has been shown to help relieve pain and inflammation by modulating the inflammatory pathways that affect heart, joints, liver, gastrointestinal tract, brain, cellular health and the immune system! This makes curcumin useful for relieving the pain in osteoarthritis, rheumatoid arthritis and bursitis as well as in digestive conditions such as ulcerative colitis, Crohn's disease, celiac disease, gastritis and gastric ulcers. Curcumin has the ability to block more than 30 different inflammation pathways! Curcumin also protects against inflammatory calcium loss from our bones and has been shown to slow prostate cell proliferation in addition to supporting healthy cholesterol and blood pressure levels. Curcumin has liver-protective effects and is a powerful liver detoxifier. It helps to prevent the build-up of toxins, enhance glutathione levels, supports bile production and solubility as well as improve digestive function. Curcumin may help reverse certain forms of liver cirrhosis to some degree, and is thought to be especially helpful for people who regularly drink alcohol or use common painkillers, both of which damage cause liver damage. Studies suggest that curcumin can also reduce the severity of liver injury induced by iron overdose, cholestasis and carbon tetrachloride intoxication. In addition to supporting the liver processes, managing inflammation is also vital in aiding detoxification. Inflammation control is needed because the detoxification process involves the release of toxic metabolites from our cells and tissues in order to expel them from the body. On the way to being eliminated, these toxins can trigger inflammatory reactions and cause tissue damage. Curcumin, was originally researched for Alzheimer's disease because studies found there is a much lower incidence and prevalence of Alzheimer's in India than in North America. The association between curry consumption and cognitive level in certain populations were researched and it was found that those who ate curry foods performed better on a standard test than those who never or rarely ate curry! Alzheimer's disease degrades the nerve cells in the brain through inflammation in glial cells, the formation of beta-amyloid plaques, metal toxicity, and oxidative damage. Curcumin acts as a powerful anti-inflammatory and antioxidant in the brain. It can also break down plaques and has the potential to guard against their development, plus it supports healthy neurotransmitter function, improving memory and helping to prevent cognitive decline.

Cellular prion protein mediates impairment of synaptic plasticity by amyloid-beta oligomers.


The Medium, November 2017
According to Uma Naidoo, turmeric is an ingredient found in curry that appears to be responsible for de-plaguing the brain. Naidoo also explains that turmeric, also referred to as "Indian gold," has properties that benefit the brain, making you almost as bright as its own fiery complexion. The ingredient responsible for this powerful herb's effects on the brain is known as curcumin. Naidoo says, “Curcumin has been found to possess neuroprotective properties, and may help shield the brain against Alzheimer’s disease (AD) by binding to and eliminating toxic beta-amyloid plaques, which are a hallmark of AD."

Amyloid-β and tau: the trigger and bullet in Alzheimer disease pathogenesis.


Amyloid hypothesis Beta Amyloid deposition

Brain inflammation is also commonplace with Alzheimer’s disease. In June 2016’s Aging and Mechanisms of Disease, members of the Salk Institute team studied nerve cells altered to produce higher levels of the amyloid beta protein in order to mimic the conditions found in Alzheimer’s. High levels of the protein are associated with cellular inflammation and higher rates of neuronal death. Previously, it was thought that the inflammation occurred from immune cells, but an uncanny discovery proved otherwise—the amyloid beta proteins instead are the cause of inflammatory effects within the brain.

Carnosine, Still the Best for Anti-Aging - Baseline of …

Signalling mechanism: from binding of Beta Amyloid to PirB to activation of cofilin
Co-immunoprecipitation of hippocampal neurons to determine binding between Pir-B, PP2A or PP2B and cofilin
Mass spectrometry for
de novo
sequencing and protein structure determination if other proteins are found to be associated with Pir-B, PP2A or PP2B and cofilin



III.

Why starting Alzheimer's disease treatment early could …

The deterioration of the brain that occurs during Alzheimer’s is due to the plaques from amyloid beta proteins clumping together. Amyloid beta is an indicator of Alzheimer’s disease, present within the brain prior to Alzheimer’s disease patients becoming symptomatic of the disease. Small clumps of this protein can block synapsing between neuronal cells.

Alzheimer's disease - Wikipedia

In the Salk Institute study spearheaded by Salk Professor David Schubert, amyloid beta protein levels exposed to high levels of THC compounds reduced the amyloid beta protein levels as well as eliminated the inflammatory response from neuronal cells caused by the protein. The reduction of amyloid beta protein levels and inflammation allow the neurons to survive. THC-like compounds, like endocannibinoids, may be involved in protecting neuronal cells from death.