Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 34,264 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.
What this blog is for:
My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
Nicotinamide adenine dinucleotide (NAD+) decline is a molecular characteristic of aging and age-associated neurodegenerative diseases. Lee and colleagues uncover an astrocyte-specific regulatory axis directed by the circadian clock component REV-ERBα, and provide proof-of-concept evidence that targeting this pathway alleviates tauopathy in mouse models.
Is this enough for your doctor to create a diet protocol on this? Or will your doctor do absolutely nothing? How else is your doctor reclaiming your 5 lost cognitive years from your stroke?
Researchers from the Lewis Katz School of Medicine at Temple
University have found that extra virgin olive oil (EVOO) could help
boost brain power and halt the progression of the effects of aging on
the brain. The study was published in the latest issue of the journal Aging Cell,
and it was titled, “Extra virgin olive oil improves synaptic activity,
short‐term plasticity, memory, and neuropathology in a tauopathy model.”
Manufacturing extra virgin Olive Oil in Mola di Bari, Puglia - Image Credit: Sabino Parente / Shutterstock
Researchers explained that EVOO is a food that is rich in
antioxidants that can benefit health in more than one way. These
antioxidants are especially beneficial for the brain and heart. This new
study follows their earlier work that shows that EVOO can help restore
memory and also protects the brain from damage caused by Alzheimer’s
disease. This study was conducted on mice at the time.
In a new study, also conducted on lab mice, reveals that EVOO can
benefit another group of dementia-related pathology called tauopathies.
An abnormal protein called tau protein can build up within the brain and
can lead to dementia and slow the decline in cognitive functions, wrote
the researchers. This study reveals that the use of EVOO can help
prevent a specific decline of the mental faculties called frontotemporal
dementia that is seen with tauopathies.
The team of researchers explained that tauopathies and dementia
affects different parts of the brain. Alzheimer’s disease, for example,
affects the hippocampus region, which deals with memory. Frontotemporal
dementia, on the other hand, affects the frontal lobe and the temporal
lobes. These are present at the forehead and sides of the head,
respectively. Frontotemporal dementia is usually seen between the ages
of 40 and 65 years and there are alterations in personality traits,
language, handwriting, behaviors, etc. With time, there is a
deterioration of memory and cognitive functions.
One of the senior researchers, Domenico Praticò, MD, Scott Richards
North Star Foundation Chair for Alzheimer's Research, Professor in the
Departments of Pharmacology and Microbiology, and Director of the
Alzheimer's Center at Temple, in his statement said, “EVOO has been a
part of the human diet for a very long time and has many benefits for
health, for reasons that we do not yet fully understand. The realization
that EVOO can protect the brain against different forms of dementia
gives us an opportunity to learn more about the mechanisms through which
it acts to support brain health.”
For
the Alzheimer’s disease study, they had used mice modeled to develop
the disease. They fed the mice on EVOO and when their brains were
dissected on death, there were no features of brain damage and deposits
of the abnormal proteins within their brains. EVOO-fed mice were also
found to have normal cognitive functions.
In this new study, they took mice that were genetically engineered
(hTau mice) to develop tauopathy or deposits of abnormal protein tau in
their brains. The tau usually forms tangles and deposits in various
parts of the brain. These tangles cause blockage in the neuron
communications and thus impair memory and thinking. In humans, this
leads to frontotemporal dementia.
Mice designed to develop tauopathies were then put on a diet of EVOO
supplementation from a young age (corresponding to age 30 to 40 years in
humans). At six months of age (corresponding to a human age of 60
years) the mice were found to have a 60% reduction in the tau protein
deposits in their brains. These mice were also found to have a 60%
reduction in the formation of damaging tau deposits in their brains. The
synapse functions were better in these mice and they also had higher
levels of a protein called complexin-1. This protein is found to be
important for maintaining healthy neural connections or synapses. They
tested the mice for memory and learning tests and found that the mice
fed on EVOO did well on those tests as well.
Our findings demonstrate that EVOO directly improves synaptic
activity, short‐term plasticity, and memory while decreasing tau
neuropathology in the hTau mice. These results strengthen the healthy
benefits of EVOO and further support the therapeutic potential of this
natural product not only for AD but also for primary tauopathies.”
Lewis Katz School of Medicine, Temple University
They wrote that the results, “provide strong preclinical evidence in
support of the novel concept that EVOO should be considered as a
potential and viable multi‐targeting agent not only for AD but also for
primary tauopathies.”
As a next step, the team plans on using EVOO in older mice and see if
it can reverse the signs of cognitive decline and reverse the tau
tangles and deposits.
We are particularly interested in knowing whether EVOO can reverse tau damage and ultimately treat tauopathy in older mice."
Dr. Praticò, Lewis Katz School of Medicine, Temple University
Journal reference:
Lauretti,
E, Nenov, M, Dincer, O, Iuliano, L, Praticò, D. Extra virgin olive oil
improves synaptic activity, short‐term plasticity, memory, and
neuropathology in a tauopathy model. Aging Cell. 2019; 00:e13076.
https://doi.org/10.1111/acel.13076, https://onlinelibrary.wiley.com/doi/full/10.1111/acel.13076
You will need this. SO DEMAND TO KNOW FROM YOUR DOCTOR AND STROKE HOSPITAL WHAT THEY ARE DOING TO ENSURE THIS CREATES A PREVENTION PROTOCOL FOR YOUR USE.
Tauopathy has been out there since July 2012. How fucking long will you allow your doctor and stroke hospital to continue this incompetence? After your children and grandchildren have strokes?
Domenico Praticò, MD, Scott Richards North Star
Foundation Chair for Alzheimer's Research, Professor in the Departments
of Pharmacology and Microbiology, and Director of the Alzheimer's Center
at Temple at the Lewis Katz School of Medicine at Temple University
Credit: Lewis Katz School of Medicine at Temple University
Like a sorting machine in an assembly line, a molecule known as
VPS35 detects and removes defective proteins from neurons. And similar
to other quality control processes, the VPS35 system goes a long way
toward protecting health, according to new work by researchers at the
Lewis Katz School of Medicine at Temple University. They show for the
first time that VPS35 clears the brain of a potentially harmful protein
called tau, which otherwise accumulates and contributes to
neurodegenerative disorders, including Alzheimer's disease.
The new findings were published online July 9 in the journal Molecular Psychiatry.
"A major part of what VPS35 does is to sort out and transport
dysfunctional proteins to degradation sites," explained senior
investigator Domenico Praticò, MD, Scott Richards North Star Foundation
Chair for Alzheimer's Research, Professor in the Departments of
Pharmacology and Microbiology, and Director of the Alzheimer's Center at
Temple at the Lewis Katz School of Medicine (LKSOM).
The buildup of defective proteins in neurons is a feature shared by
Alzheimer's disease, Parkinson's disease, and several other
neurodegenerative conditions. Tau is one of the major proteins to amass
in the brain and cause damage in these diseases, creating a condition described as tauopathy.
Previous work by other researchers had shown that the function of
VPS35 is altered in Alzheimer's disease and that VPS35 activity is
reduced in the brains of Alzheimer's patients. The relationship between
VPS35 activity and tau accumulation was largely unexplored.
"We asked specifically whether the VPS35 system is important for
clearing defective tau proteins," Dr. Praticò said. To answer this
question, his team of researchers examined brain tissue from patients
with either progressive supra-nuclear palsy (PSP) or Picks' disease.
Unlike Alzheimer's disease, in which tau accumulation is secondary to
that of beta-amyloid, in PSP and Picks' disease tau is the only protein to form deposits in the brain.
Analyses revealed that the brains of PSP and Pick's disease patients
had VPS35 levels that were 50 percent lower than those of control
subjects. When the researchers deliberately altered VPS35 levels in
individual tauopathy-affected neurons in vitro, they discovered that
they could directly control tau accumulation, for the first time
implicating VPS35 in tauopathy. The VPS35-dependent effect on tau was
mediated by the activity of cathepsin D, an enzyme that specializes in
protein degradation.
Dr. Praticò's team also carried out experiments in mice with tau
accumulation. VPS35 downregulation in these animals exacerbated memory
and learning impairment and was associated with worsened motor function.
Moreover, VPS35 reduction resulted in a loss of synaptic integrity
between neurons in the animals' brains, significantly damaging neural
communication.
"When tau lingers in cells, it is very bad for synapses, the places
where neurons meet and exchange signals," explained Dr. Praticò. "In the
animals we studied, there was a 40 to 50 percent loss in synaptic
connectivity when VPS35 activity was reduced, which led to the types of
cognitive and motor deterioration, including losses in memory and
learning ability, seen in human tauopathy patients."
The discovery of the involvement of cathepsin D shed additional light
on the relationship between VPS35 and tau. "Without VPS35, cathepsin D
does not degrade tau, leaving tau to build up in the brain," Dr. Praticò
said.
Dr. Praticò's team plans next to investigate the possibility of using
a drug to put VPS35 back to work in the context of neurodegenerative
disease. "The approach would be unique. Instead of targeting an enzyme,
as other small molecules have been developed to do, we would be
targeting an actual mechanism, which should be more viable," he said.
What is your doctor doing to make sure your BDNF is high enough to prevent neurodegeneration? Or is s/he waiting for decades for human research to be done? Thus dooming you to dementia/Alzheimers. If you won't go down without a fight you will need to start screaming at your doctors for help in solving this problem. Now, not 50 years from now. https://espace.library.uq.edu.au/view/UQ:413018
Jiao, S.-S., Shen, L.-L., Zhu, C., Bu, X.-L., Liu, Y.-H., Liu,
C.-H., Yao, X.-Q., Zhang, L.-L., Zhou, H.-D., Walker, D. G., Tan, J.,
Götz, J., Zhou, X.-F. and Wang, Y.-J. (2016) Brain-derived neurotrophic
factor protects against neurodegeneration in a mouse model of human
tauopathy. Translational Psychiatry, 610: . doi:10.1038/tp.2016.186
Abstract
Reduced expression of brain-derived neurotrophic
factor (BDNF) has a crucial role in the pathogenesis of Alzheimer’s
disease (AD), which is characterized with the formation of neuritic
plaques consisting of amyloid-beta (Aβ) and neurofibrillary tangles
composed of hyperphosphorylated tau protein. A growing body of evidence
indicates a potential protective effect of BDNF against Aβ-induced
neurotoxicity in AD mouse models. However, the direct therapeutic effect
of BDNF supplement on tauopathy in AD remains to be established. Here,
we found that the BDNF level was reduced in the serum and brain of AD
patients and P301L transgenic mice (a mouse model of tauopathy).
Intralateral ventricle injection of adeno-associated virus carrying the
gene encoding human BDNF (AAV-BDNF) achieved stable expression of BDNF
gene and restored the BDNF level in the brains of P301L mice.
Restoration of the BDNF level attenuated behavioral deficits, prevented
neuron loss, alleviated synaptic degeneration and reduced neuronal
abnormality, but did not affect tau hyperphosphorylation level in the
brains of P301L mice. Long-term expression of AAV-BDNF in the brain was
well tolerated by the mice. These findings suggest that the gene
delivery of BDNF is a promising treatment for tau-related
neurodegeneration for AD and other neurodegenerative disorders with
tauopathy.
Another word to learn - tauopathy
We need to know about this since we as stroke survivors have a higher risk of getting Alzheimers. But ask your doctor what you can do to prevent that higher risk. http://www-06.all-portland.net/bst/040/0656/0400656.pdf
Tauopathies are neurodegenerative diseases, including AD (Alzheimer's
disease) and FTLD-T (tau-positive frontotemporal lobar degeneration),
with shared pathology presenting as accumulation of detergent-insoluble
hyperphosphorylated tau deposits in the central nervous system. The
currently available treatments for AD address only some of the symptoms,
and do not significantly alter the progression of the disease, namely
the development of protein aggregates and loss of functional neurons.
The development of effective treatments for various tauopathies will
require the identification of common mechanisms of tau neurotoxicity,
and pathways that can be modulated to protect against neurodegeneration.
Model organisms, such as Caenorhabditis elegans, provide methods
for identifying novel genes and pathways that are involved in tau
pathology and may be exploited for treatment of various tauopathies. In
the present paper, we summarize data regarding characterization of MSUT2
(mammalian suppressor of tau pathology 2), a protein identified in a C. elegans
tauopathy model and subsequently shown to modify tau toxicity in
mammalian cell culture via the effects on autophagy pathways. MSUT2
represents a potential drug target for prevention of tau-related
neurodegeneration.
