Bleeding Edge

Apparently the process of neurodegeneration is the root cause of very many autoimmune system failures and related cancers, and other lymphomas, like Non-Hodgins lymphoma, and also for more directly linked illness such as Alzheimers, Lou Gehring disease, Dementia, Forgetfulness, and a host of other severe neurological brain illnesses that assault and ravage our people today.

It is the bridge building process of the cranial brain and the human primary neurology, whereas the synaptic connections between neurons are in a constant state of flux between birth and adulthood — and that is the processing brain activity that fails the affected hundreds of millions of humans, most often.

Because, as new synapses are built, a complementary biological system of our neurological tree and the brain stem — works hard in order to finetune the whole of the brain by erasing other older and far less often usedAdvance Life Science Venture Capital
synaptic electrical switches that we call “connections”.

And this is seen as the crucial first step for the process, known as “synaptic pruning” that in turn is crucial for further brain development as it involves a part of our immune system called the classical complement pathway.

And because this connection to our primary classical Immune system is a massive discovery in and of itself… as it allows us to have new targeted proteins for

Yet there is even a slew of further evidence that “defects” in the pruning may be involved in neuro-developmental disorders such as madness, alcoholism, opioids, & other drug addictions, schizophrenia, and even autism and mongolism.

We know that now, because the new studies have found that the same synaptic pruning systems that are present in the early stages of the baby’s and the children’s neurodevelopment — fully reactivate later on in life as the pr primary progression of neurodegenerative diseases, such as Autoimmune diseases, Self directed cancers, Dementias, Alzheimer’s and all the rest of it’s ilk of illnesses, are growing in the lives of modern long living people.

Today ALS-VC recognizes that these fresh neurological findings may offer a long-sought mechanism for synapse loss that is crucial in these diseases, and thus we open the door to a potential new therapeutic approach to combat certain types of neurodegeneration through the complementarity of the sought after proteins that will balance the neurological synaptic pruning process all over again.

Because back in November of 2018, a study was published of an experimental trial run by a team of researchers that was led by Morgan Sheng noted neuroscientist, and Borislav Dejanovic a neuroscience postdoctoral fellow, and it was reported in the magazine Neuron, that a single protein in the complementary pathway, called complement component 1q, or C1q, is abundant in the brain of preclinical models that mimic the “tau pathology” seen in all of the Alzheimer’s and other neurodegenerative diseases, and autoimmune disease patients…

Naturally this protein is created or “manufactured and released” by the brain’s specific immune cells, called microglia.

Further research indicates that “C1q” protein plays a most important and essential role in neurodevelopmental and on the regulation of the “synaptic pruning” process.

But in “tau pathologies” the protein “C1q” may also lead to the accelerated decay of synapses crucial for the proper brain functions of all of our brains.

Therefore, the neuroscientific research team’s discovery, suggests that “C1q-blocking antibodies” reduced the removal of synapses by microglia during that synaptic removal process known as synaptic pruning, and thus rescued synapse density in mice. The study also found elevated C1q levels in the synapses of Alzheimer’s patients, suggesting that the complement pathway is reactivated in neurodegenerative disease.

Taking the research a step further, a study led by Jesse Hanson and Tiffany Wu, published in August 2019 in “Cell Reports” showed that blocking C3, another key protein in the same complement pathway, similarly rescued synapse density and neuron loss in mice with “tau pathologies.” The team also found that C3, like C1q, was expressed in the microglia of these mice and elevated in the synapses of Alzheimer’s patients.

Together, the studies offer encouraging evidence that targeting microglial synapse removal through the complement pathway might help slow the progression of Alzheimer’s and other tau-associated neurodegenerative diseases that appear later in life.

And that my friends, is the Great News for hundreds of millions of people around the Earth that are affected by these autoimmune failures and related diseases…

Well Done and it would appear that the ALS-VC mission is quite clear here.

Yours,

Dr Churchill

PS:

Should you want to learn more about our exciting work in the area of synaptic, neuron and neurological degeneration, and beyond, please reply herewith or at http://www.ALSVC.com and communicate with us.

PPS:

We are also actively seeking brilliant minds and motivated scientists and business people that want to heal the world…

PPPS:

For people who seek advanced therapies in this field and are willing to enlist in extremely advanced and experimental trials of novel medications — please contact us through the website and we shall direct you accordingly to the companies that perform some of the most promising clinical trials today.