THC reverses Amyloid-beta build up.

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I had to make this video just to show my brother that we must try and fix our mum.
Information takes time, we don’t have time.
A team of Cleveland Clinic Lerner Research Institute researchers led by Riqiang Yan, PhD, Department of Neurosciences, found that gradually depleting an enzyme called BACE1 completely reverses the formation of amyloid plaques in the brain and improves cognitive function in mice with Alzheimer’s disease, correcting both the brain pathology and symptoms most commonly associated with the disease. The study, which was published February 14 in the Journal of Experimental Medicine, raises hopes that drugs targeting this enzyme will successfully treat Alzheimer’s in humans.
“When we were able to identify the molecular basis of the inflammatory response to amyloid beta, it became clear that THC-like compounds that the nerve cells make themselves may be involved in protecting the cells from dying,” explains Currais.
Prescription of a THC/CBD-Based Medication to Patients with Dementia: A Pilot Study in Geneva
Broers B.a · Patà Z.b · Mina A.b · Wampfler J.c · de Saussure C.c · Pautex S.d
Author affiliations
Corresponding Author
Keywords: CannabinoidsDementiaTreatmentTHC/CBD

Med Cannabis Cannabinoids 2019;2:56–59

Know Your Compounds
Despite their similar molecular structures, the two main compounds in marijuana — tetrahydrocannabinol (THC) and cannabidiol (CBD) — have different effects in the human body.
THC: An active ingredient in marijuana that makes you high, THC binds to CB1 receptors in the brain to create a euphoric effect.
CBD: This compound in cannabis is non-psychoactive, meaning it won’t give you a high. It has little affinity for binding with the CB1 or CB2 receptors, and can actually hinder THC’s effects when combined. Instead, CBD can activate other receptors, such as serotonin, and is more often sought out for its potential medicinal benefits, such as pain and anxiety relief.
Amyloid proteotoxicity initiates an inflammatory response
blocked by cannabinoids.

Endocannabinoids can be produced in response to stress,
and in rodent AD models cannabinoids reduce Aβaccumulation
and improve memory. THC also reduces inducible huntingtin
overexpression in PC12 cells, and both THC and endocannabi-
noids reduce inflammation. Several synthetic, plant derived
and endogenous cannabinoids are able to prevent the accumula-
tion of intraneuronal Aβ, reduce the production of eicosanoids,
and block nerve cell death. Therefore, it is reasonable to conclude
that there is a therapeutic potential of cannabinoids for the
treatment of AD.
A Review on Studies of Marijuana for Alzheimer’s Disease – Focusing on CBD, THC
BACE1 initiates the generation of the β-amyloid peptide, which likely causes Alzheimer’s disease (AD) when accumulated abnormally. BACE1 inhibitory drugs are currently being developed to treat AD patients. To mimic BACE1 inhibition in adults, we generated BACE1 conditional knockout (BACE1fl/fl) mice and bred BACE1fl/fl mice with ubiquitin-CreER mice to induce deletion of BACE1 after passing early developmental stages. Strikingly, sequential and increased deletion of BACE1 in an adult AD mouse model (5xFAD) was capable of completely reversing amyloid deposition. This reversal in amyloid deposition also resulted in significant improvement in gliosis and neuritic dystrophy. Moreover, synaptic functions, as determined by long-term potentiation and contextual fear conditioning experiments, were significantly improved, correlating with the reversal of amyloid plaques. Our results demonstrate that sustained and increasing BACE1 inhibition in adults can reverse amyloid deposition in an AD mouse model, and this observation will help to provide guidance for the proper use of BACE1 inhibitors in human patients.


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