The tau protein alphabetic character macromolecules AR a bunch of six extremely soluble macromolecule isoforms made by various junction from the sequence MAPT (microtubule-associated protein tau).
Mutated Tau Proteins and Neurodegeneration
The human brain contains over 100 billion neurons. These neurons are some of the longest-lived cellsin the human body, each one connectedto upwards of 10,000 others.
Seamless communication between these neurons allows the nervous system to carry out a multitude of functions. At the neuron’s nucleus, an individual’s genetic information is processed and stored in the form of DNA.
A structure called the nuclear pore complex allows for proteins, RNA, and other small molecules to pass from the nucleus to the rest of the cell, and back again.
This process is a crucial component of most living cells, including our nervous system. Without a healthy, functioning nuclear pore complex, traffic jams build up in the cell, which may make people susceptible to neurodegenerative conditions like Huntington’s disease, ALS, Parkinson’s, or others.
Scientists have recently identified a link between certain mutated proteins, and dysfunction at the nuclear pore complex. One particular protein, called Tau, has been identified accumulating in the brains of individuals with Alzheimer’s, and it’s suspected to cause traffic jams or blockages between the nucleus and the rest of the cell.
Researchers found that in the presence of a mutated version of the Tau protein, the nuclear pores become physically disrupted, fewer in number, and pieces coalesce with each other. The hope is that scientists can address the root cause behind the damaged nuclear pores, or find a way to stabilize them.
This may help researchers to develop treatments that allow the cell to function normally, restoring the flow of traffic in and out of the nucleus, ultimately treating the disease.
Tau Protein Pathology in Alzheimer’s Disease
the healthy brain has around 86 billion interconnected neurons which communicate using electrical and chemical signals tang protein through binding at its repeat domain supports microtubules needed for cell structure.
and to provide rapid transit pathways for vesicles mitochondria and cell components to the synaptic junction aging brain neurons lose some ability to clear waste material which can accumulate as lipofuscin where tau can bind and misfold, misfolded tau can capture normal tau causing it to misfold in the same way.
and form oligomers which disrupt the synapse tau oligomers can transfer to other neurons and initiate the same process of tau capture causing the disease to spread as oligomers aggregate and grow they form paired helical filaments and then bundles called tangles as neurons fill up with tangles they can no longer function properly and eventually burst to leave behind just tangles.
Alzheimer’s researchers focus on Tau protein
ON THE ADMIRAL’S COMMENTS SOFAR. AMONG OLDER ADULTS, ALZHEIMER’S DISEASE IS THE MOST COMMON FORM OF DEMENTIA, A PROGRESSIVE DISORDER THAT DESTROYED DESTROYS BRAIN HUNKS U. FUNCTION.
FOR MANY YEARSSCIENTISTS HAVE FOCUSED ONAMYLOID PLAQUE THAT FORMS IN THEBRAIN OF APPLES PATIENTS.NOW THE ATTENTION IS TURNING TOSOMETHING NEW.IT’S ANOTHER PROTEIN, THIS ISONE CALLED YOU TO.
THEY’VE ALREADY DONEIMMUNIZATIONS AND VACCINESAGAINST THE AMYLOID WHICH HASN’TSHOWN TO BE ANY EFFECT BUT NOWWE CAN DO THINGS AGAINST TOU.YOU CAN DO THINGS SIMILAR TO TAMYLOID BUT AGAINST TOU AND WETHINK THAT IS GOING TO REVERSETHE ALZHEIMER’S DISEASE.
DR. HILLARY GRAZER ANEUROLOGIST WITH MEMORIAL HEALTHCARE SHE HAD HOPES TO JOIN INNEW CLINICAL TRIALS THAT AREUNDERWAY RIGHT NOW THAT AREUSING PET SCANS TO LOOK FOREVIDENCE OF THIS TR HAVEOU FRONTIN THE BRAIN.
AND ANOTHER OPTION FOR DETECTINGALZHEIMER’S MAY LIE IN THE BONE,NOT THE BRIN.RESEARCHERS HAVE FOUND YOU LINKBETWEEN EARLY BONE LOSS ANDBRAIN DEGENERATION.FEWER THAN 5% OF CASES OFALZHEIMER’S DISEASE HAVE’S CLEARGENETIC, AND YOU THAT MAKESFINDING NEW BY OH MARKERS SO.
Dr. Alexa Woo groundbreaking research on tau proteins
Alexa Woo, PhD, an assistant professor of molecular pharmacology and physiology at the Byrd Alzheimer’s Institute, research focuses on preventing tau proteins from malfunctioning. When tau malfunction, it can eventually lead to neurodegenerative diseases including Alzheimer’s disease.
Neurofibrillary tangles and Tau protein (Alzheimer)
let’s start with neurofibrillary tangles as part of the cytoskeleton microtubules play an important role in the formation of cell shape and transportation of important nutrients within the nerve cells.
in healthy neurons there is a natural protein called tau protein which maintains the integrity of cellular microtubules, however in Alzheimer disease the TEL proteins are abnormally high professor related.
this hyper phosphorylation process makes our proteins inactive and as a result the microtubule loses its natural integrity and starts to collapse.
the hyper phosphorylated tell proteinaggregates to form new pathologicalstructures called neurofibrillarytangles which distribute throughout bodynerve cells.
To recap my top picks:
- Mutated Tau Proteins and Neurodegeneration
- Tau Protein Pathology in Alzheimer’s Disease
- Alzheimer’s researchers focus on Tau protein
- Dr. Alexa Woo groundbreaking research on tau proteins
- Neurofibrillary tangles and Tau protein (Alzheimer)
What does protein tau do?
Tau may be a super molecule that helps stabilize the inner skeleton of nerve cells (neurons) within the brain. This internal skeleton incorporates a tube-like form through that nutrients and alternative essential substances jaunt reaches completely different elements of the vegetative cell.
How is u003cstrongu003etau proteinu003c/strongu003e detected?
Tau and different biomarkers are often detected with PET scans of the brain and work tests of cerebrospinal fluid. However, PET imaging is dear and involves hot agents, and cerebrospinal fluid tests need spinal faucets, that square measure invasive, complicated, and long. Less complicated biomarker tests square measure still required.
How does tau protein cause Alzheimer’s?
In Alzheimer’s, however, abnormal chemical changes cause letter of the alphabet to detach from microtubules and keep on with alternative letter of the alphabet molecules, forming threads that eventually be a part of to create tangles within neurons. These tangles block the neuron’s transport system, that harms the col ligation communication between neurons.