Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 34,370 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.
Analyzing data from 8 anti-amyloid antibodies and 23,202 subjects, you'd need a magnifying glass to see something good. The conclusion is disarmingly simple: the benefits are imperceptible. Removing amyloid in #Alzheimers is not worth the risks.
PURPOSE
We conducted a meta-analysis to evaluate clinically meaningful benefits
and harms of monoclonal antibodies targeting amyloid in patients with
Alzheimer dementia.
METHODS
We searched PubMed, Cochrane CENTRAL, and 5 trial registries, as well
as the reference lists of identified studies. We included randomized
controlled trials comparing a monoclonal antibody with placebo at a dose
consistent with that used in phase 3 trials or for Food and Drug
Administration approval. Studies had to report at least 1 clinically
relevant benefit or harm. Data were extracted independently by at least 2
researchers for random effects meta-analysis. Changes in cognitive and
functional scales were compared between groups, and each difference was
assessed to determine if it met the minimal clinically important
difference (MCID).
RESULTS
We identified 19 publications with 23,202 total participants that
evaluated 8 anti-amyloid antibodies. There were small improvements over
placebo in the Alzheimer’s Disease Assessment Scale (ADAS)-Cog-11 to -14
score (standardized mean difference = −0.07; 95% CI, −0.10 to −0.04),
Mini Mental State Examination score (0.32 points; 95% CI, 0.13 to 0.50),
and Clinical Dementia Rating-Sum of Boxes scale score (mean difference
=−0.18 points; 95% CI, −0.34 to −0.03), and the combined functional
scores (standardized mean difference = 0.09; 95% CI, 0.05 to 0.13). None
of the changes, including those for lecanemab, aducanumab, and
donanemab, exceeded the MCID. Harms included significantly increased
risks of amyloid-related imaging abnormalities (ARIA)-edema (relative
risk [RR] = 10.29; number needed to harm [NNH] = 9), ARIA-hemorrhage (RR
= 1.74; NNH = 13), and symptomatic ARIA-edema (RR = 24.3; NNH = 86).
CONCLUSIONS
Although monoclonal antibodies targeting amyloid provide small benefits
on cognitive and functional scales in patients with Alzheimer dementia,
these improvements are far below the MCID for each outcome and are
accompanied by clinically meaningful harms.
You'll want this test so you can implement your doctor's EXACT DEMENTIA PREVENTION PROTOCOLS. Oh your doctor doesn't have one, well then you have an incompetent doctor who doesn't know about the Bredesen Protocol or anything else?
First in vitro diagnostic to detect amyloid in early disease setting
by
Judy George, Senior Staff Writer, MedPage Today
May 5, 2022
The first in vitro diagnostic tool to help detect early Alzheimer's disease was authorized by the FDA on Wednesday.
The assay measures the ratio of beta-amyloid 1-42 to beta-amyloid
1-40 in cerebrospinal fluid (CSF). The Lumipulse G ß-Amyloid Ratio
(1-42/1-40) test is intended to be used in adults 55 and older
presenting with cognitive impairment who are being evaluated for
Alzheimer's disease or other causes of cognitive decline.
Test results are consistent with amyloid PET scan results, the agency noted.
"The availability of an in vitro diagnostic test that can potentially
eliminate the need for time-consuming and expensive PET scans is great
news for individuals and families concerned with the possibility of an
Alzheimer's disease diagnosis," said Jeff Shuren, MD, JD, director of
the FDA's Center for Devices and Radiological Health, in a statement.
"With the Lumipulse test, there is a new option that can typically be
completed the same day and can give doctors the same information
regarding brain amyloid status, without the radiation risk, to help
determine if a patient's cognitive impairment is due to Alzheimer's
disease," Shuren added.
The FDA evaluated the safety and effectiveness of the Lumipulse test
in a clinical study of 292 CSF samples from the Alzheimer's Disease
Neuroimaging Initiative (ADNI) cohort, which were compared with amyloid
PET scan results.
Overall,
97% of ADNI participants with positive Lumipulse results had the
presence of amyloid plaques on PET, and 84% of individuals with negative
Lumipulse results had a negative amyloid scan, the agency said.
Risks associated with the test include the possibility of false
positive or false negative results. "Importantly, the Lumipulse G
β-amyloid Ratio (1-42/1-40) is not a stand-alone test and other clinical
evaluations or additional tests should be used for determining
treatment options," the FDA pointed out.
There's an unmet need for a reliable, safe test to identify patients
with amyloid plaques consistent with Alzheimer's disease, the agency
added. Amyloid plaques can occur in other diseases but being able to
detect their presence, along with other evaluations, can help clinicians
determine the probable cause of a patient's symptoms.
Much research in recent years has focused on blood as a new matrix for Alzheimer's biomarkers that already have been validated in CSF. A blood test for amyloid-beta
has been widely available in the U.S. since 2020 under a CMS
certification process for laboratories that tests patient samples, but
is not yet FDA-approved.
FDA
permitted marketing of the Lumipulse G ß-Amyloid Ratio (1-42/1-40) test
to Fujirebio Diagnostics. The agency reviewed the assay through its de novo
premarket review pathway. This action creates a new regulatory
classification, which means that subsequent devices of the same type
with the same intended use can obtain marketing authorization by
demonstrating substantial equivalence to a predicate device.
Judy George
covers neurology and neuroscience news for MedPage Today, writing about
brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy,
autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep,
pain, and more. Follow
The F.D.A. has so far imposed strikingly few limitations on Aduhelm, a
monthly intravenous infusion that requires patients to have regular
M.R.I. scans because the drug can cause swelling or hemorrhaging in the
brain.
So while at the hospital your doctor needs to monitor your sleep to make sure you get to deep sleep. I'm not sure sleeping pills do that. THIS IS YOUR DOCTOR'S RESPONSIBILITY!
There's growing evidence that a lack of deep sleep increases
the risk of Alzheimer's disease. Scientists say that's because during
deep sleep, the brain removes toxins associated with Alzheimer's.
ARI SHAPIRO, HOST:
We continue to learn about the connection between sleep and
Alzheimer's disease. NPR's Jon Hamilton brings us this report done with
the NPR science podcast Short Wave.
JON HAMILTON, BYLINE: There's growing evidence that people who
don't sleep well are more likely to develop Alzheimer's. Matthew Walker
at the University of California, Berkeley, says that's no coincidence.
MATTHEW WALKER: We are now learning that there is a significant
relationship between sleep and dementia, particularly Alzheimer's
disease.
HAMILTON: Walker says the strongest evidence involves deep sleep.
That's a time when dreams are rare, body temperature drops and the
brain produces slow, rhythmic electrical waves.
WALKER: There is something about this deep sleep that is helping protect you against amyloid buildup in the brain.
HAMILTON: Amyloid or beta amyloid is a substance that forms
sticky clumps in the brains of people who are likely to develop
Alzheimer's. So Walker had a question.
WALKER: Can I look into your future and can I accurately estimate
how much beta amyloid you're going to accumulate over the next two
years, the next four years, the next six years, simply on the basis of
your sleep tonight?
HAMILTON: To find out, Walker and a team studied 32 older adults
who had taken part in a sleep study. None had memory problems. The
scientists used brain scans to track levels of beta amyloid in each
participant for up to six years. And Walker says the results, published
early this month in the journal Current Biology, showed people who got
less deep sleep had more beta amyloid.
WALKER: We have a specific sleep signature right now that seems
to help us better understand where you may sit on the Alzheimer's
disease risk trajectory in the future.
HAMILTON: Scientists also have some ideas about why deep sleep
can reduce amyloid. In 2013, a study of mice found that their brains
switched on a sort of dishwasher during sleep. Laura Lewis, a biomedical
engineer at Boston University, says that appears to clear out waste
products.
LAURA LEWIS: So things like amyloid beta, which are implicated in
Alzheimer's disease, seem to actually be removed more rapidly from the
brain when an animal is asleep versus when they're awake.
HAMILTON: In 2019, Lewis led a team that showed how this dishwasher works in people.
LEWIS: We realized that there's these waves of fluid flowing into the brain during sleep.
HAMILTON: What's more, each wave of fluid was preceded by a
large, slow electrical wave. So now scientists are looking for ways to
induce the slow waves that signal deep sleep. Lewis says it's easy in
rodents.
LEWIS: There's a specific deep brain structure that if you stimulate it, you can cause these sleeplike slow waves in the brain.
HAMILTON: There's some evidence that rhythmic sounds can increase
slow waves in people. And researchers at Washington University in St.
Louis showed that treating a sleep disorder also helped. Dr. Yo-El Ju
was part of a team that studied patients with sleep apnea.
YO-EL JU: They seem to have a change in their ability to clear
proteins or, you know, waste products from their brain. And people with
obstructive sleep apnea are at higher risk for dementia down the line.
HAMILTON: So Ju's team looked to see what happened after
treatment allowed better sleep. The result - more deep sleep and more
beta amyloid cleared from the brain. And Ju says there was another
effect - participants' brains began making less beta amyloid.
JU: So I don't know whether it's that sleep increases clearance or whether sleep decreases the production of waste products.
HAMILTON: Either way, Ju says sleep is important to brain health, though on the day we spoke, she hadn't gotten that much.
JU: My 2-year-old decided to sleep in my bed and eat a tortilla
and a banana at 2 in the morning. But usually, I get a pretty good
sleep.
NPR transcripts are created on a rush deadline by Verb8tm, Inc.,
an NPR contractor, and produced using a proprietary transcription
process developed with NPR. This text may not be in its final form and
may be updated or revised in the future. Accuracy and availability may
vary. The authoritative record of NPR’s programming is the audio record.
My reading between the lines would suggest that you vastly increase cerebal blood flow.
But what EXACTLY is the best way to get better blood flow? And wouldn't
you immediately want better blood flow to your brain now to try to prevent Alzheimer's?
So ask your doctor for EXACT PROTOCOLS
to increase blood flow. These posts contain my writings and ideas on increasing
blood flow. DO NOT FOLLOW THEM, I'M NOT MEDICALLY TRAINED. Your doctor
supposedly is, so ask him/her.
Daniel Albrecht, A. Lisette Isenberg, Joy Stradford, Teresa Monreal, Abhay Sagare, Maricarmen Pachicano, Melanie Sweeney, Arthur Toga, Berislav Zlokovic, Helena Chui, Elizabeth Joe, Lon Schneider, Peter Conti, Kay Jann, Judy Pa and for the Alzheimer Disease Neuroimaging Initiative
Journal of Neuroscience 12 October 2020, JN-RM-1230-20; DOI: https://doi.org/10.1523/JNEUROSCI.1230-20.2020
Tau
pathology and vascular dysfunction are important contributors to
Alzheimer’s Disease (AD), but vascular-tau associations and their
effects on cognition are poorly understood. We investigated these
associations in male and female humans by conducting voxelwise
comparisons between cerebral blood flow (CBF) and tau positron emission
tomography (PET) images in independent discovery (cognitively normal
(CN): 19; mild cognitive impairment (MCI)-risk: 43; MCI: 6) and
replication (CN: 73; MCI:45; AD: 20) cohorts. In a subgroup, we assessed
relationships between tau and soluble platelet-derived growth factor
beta (sPDGFRβ), a CSF marker of pericyte injury. We tested whether
CBF/sPDGFRβ-tau relationships differed based on Montreal Cognitive
Assessment (MoCA) global cognition performance, or based on amyloid
burden. Mediation analyses assessed relationships between CBF/sPDGFRβ,
tau, and cognition.
Negative CBF-tau correlations were
observed predominantly in temporal-parietal regions. In the replication
cohort, early negative CBF-tau correlations increased in spatial extent
and in strength of correlation with increased disease severity. Stronger
CBF- and sPDGFRβ-tau correlations were observed in participants with
greater amyloid burden and lower MoCA scores. Importantly, when
stratifying by amyloid status, stronger CBF-tau relationships in
individuals with lower MoCA scores were driven by amyloid-positive
participants. Tau PET was a significant mediator CBF/sPDGFRβ-MoCA
relationships in numerous regions.
Our results
demonstrate vascular-tau associations across the AD spectrum and suggest
that early vascular-tau associations are exacerbated in the presence of
amyloid, consistent with a two-hit model of AD on cognition.
Combination treatments targeting vascular health, as well as amyloid-β
and tau levels, may preserve cognitive function more effectively than
single-target therapies.
SIGNIFICANCE
Emerging
evidence demonstrates a role for vascular dysfunction as a significant
contributor to Alzheimer’s pathophysiology. However, associations
between vascular dysfunction and tau pathology, and their effects on
cognition remain poorly understood. Multimodal neuroimaging data from
two independent cohorts were analyzed to provide novel in vivo
evidence of associations between cerebral blood flow (CBF), an MRI
measure of vascular health, and tau pathology using PET. CBF-tau
associations were related to cognition and driven in part by amyloid
burden. Soluble platelet-derived growth factor beta (sPDGFRβ), an
independent CSF vascular biomarker, confirmed vascular-tau associations
in a subgroup analysis. These results suggest that combination
treatments targeting vascular health, amyloid-β, and tau levels, may
more effectively preserve cognitive function than single-target
therapies.
You'll have to ask you doctor what this means in layperson terms. Or I guess we could ask our fucking failures of stroke associations. But they know absolutely nothing.
This article has been accepted for publication and
undergone full peer review but has not been through the copyediting,
typesetting, pagination and proofreading process, which may lead to
differences between this version and the Version of Record. Please cite
this article as https://doi.org/10.1002/mnfr.202000632
Abstract
Scope: Alzheimer's Disease (AD) is a
neurodegenerative condition marked by the formation and aggregation of
amyloid‐β (Aβ) peptides. There exists, to this day, no cure or effective
prevention for the disease; however, there is evidence that a healthy
diet and certain food products can slow down first occurrence and
progression of peptide aggregates. To investigate if food ingredients
can interact with peptide aggregates in membrane mimics, we prepared
synthetic membranes that contained aggregates consisting of cross‐β
sheets of Aβ25–35.
Methods and Results: We studied the impact of
resveratrol, found in grapes, caffeine, ingredient in coffee,
β‐carotene, found in orange fruits and vegetables, and Epigallocatechin
gallate (EGCG), a component of green tea, on the size and volume
fraction of Aβ aggregates using optical and fluorescence microscopy,
X‐ray diffraction, UV‐Visible spectroscopy, and Molecular Dynamics (MD)
simulations. All compounds were found to be membrane active and
spontaneously partitioned in the synthetic brain membranes. While
resveratrol and caffeine led to membrane thickening and reduced membrane
fluidity, β‐carotene and EGCG preserved or increased fluidity.
Conclusion: Resveratrol and caffeine did not reduce
the volume fraction of peptide aggregates while β‐carotene significantly
reduced plaque size. Interestingly, EGCG dissolved peptide aggregates
and significantly decreased the corresponding cross‐β and β‐sheet
signals.
But is this the correct path to go down or should tau proteins be
addressed? Is this just cleaning up existing plaque but not addressing
new plaque being generated by tau? Cause and effect once again. Ask your doctor to clarify.
Trials
have demonstrated aducanumab helps to untangle Alzheimer’s tell-tale
protein clumps in the brain, potentially reversing the disease.
The FDA has not considered a new treatment for the condition in 17 years, with aducanumab’s fate being decided by 7 March 2021.
If licensed, it would be the first therapy approved to delay Alzheimer’s progression.
Existing Alzheimer's drugs work to ease symptoms. (Getty Images)
‘A new era for Alzheimer’s treatments’
“The
FDA’s acceptance of the aducanumab with priority review is an important
step in the path to potentially having a treatment that meaningfully
changes the course of Alzheimer’s disease,” said Michel Vounatsos, CEO
of the manufacturer Biogen, as reported by Global News Wire.
“We
believe aducanumab marks the beginning of a new era of potential
treatments for Alzheimer’s disease that will inspire even more discovery
and innovation to bring hope to those affected by this devastating
disease.”
“I
am heartened by what this progress may mean for people living with
Alzheimer’s disease and their families,” said Dr Christopher van Dyck,
from the Yale Alzheimer’s Disease Research Center.
“If aducanumab
is determined to be effective in reducing the decline in cognition and
activities of daily living resulting from progression of this disease by
addressing the underlying disease pathology, it will deliver meaningful
benefits to those who most need them.”
Keeps patients ‘in a better place for a longer time’
Aducanumab has had a bumpy road. Studies were scrapped in March 2019 after two late-stage trials suggested it was of no benefit.
Several months later, Biogen looked at a larger amount of data that became available after the trials stopped.
It found the drugs were effective providing they were given early enough and at a sufficient dose.
Experts
hope aducanumab will benefit those with early signs of dementia,
helping to halt or slow the disease before patients became
incapacitated.
The FDA has been set an “action date” of 7 March 2021, but “plans to act early on this application under an expedited review”.
Michael
Yee, an analyst at the investment bank Jefferies, expects a verdict in
the first quarter of 2021, adding the data demonstrating the drug’s
effectiveness is “mixed and still inconclusive”, Fierce Biotech reported.
Nevertheless,
the fast-track approval suggests the FDA is “comfortable with the
totality of the data, recognises high unmet need and really wants to get
an Alzheimer’s drug approved”, he added.
Analyst Brian Abrahams, from RBC Capital Markets, has given aducanumab a 30% chance of approval.
Dr Dennis Selkoe from Harvard told wbur:
“I think there’s a reasonable chance that aducanumab, if approved and
we don’t know that yet, will be the first disease-modifying agent for
Alzheimer’s, and that will be a huge milestone, and patients of mine and
others can access the drug.
“Having cared for hundreds of patients with this disease, this would be a game changer.
“At
least for some of my patients, if aducanumab is approved, [it would be]
something that will slow down their deterioration, that will keep them
in a better place for a longer time.”
The FDA only accepts drugs
for priority review if they offer major advances in treatments or
provide a therapy where none existed.
If approved in the US, experts are confident other health watchdogs around the world will consider doing the same.
In
the meantime, Biogen is planning further studies, which will offer high
doses to all eligible participants from the earlier trials.
Have your doctor analyze all these posts and put together a protocol to become a super ager. YOUR DOCTOR'S RESPONSIBILITY! At least if they are competent. This is not well done, YA is used but not described.
2Institute for Neuroscience and Medicine II - Molecular Organization of the Brain Research Center Juelich Juelich Germany
3German Center for Neurodegenerative Diseases Bonn/Cologne Germany
Abstract
Objectives:
The phenomenon of selected individuals cognitively performing above
the norm even at high age (so-called super-agers) suggests
that these individuals must obtain extraordinary
resistance mechanisms against brain aging processes and/or
neurodegeneration.
However, not much is known about age-associated
molecular hallmarks of neurodegeneration in super-agers, particularly
concerning
proteinopathies such as the accumulation of
amyloid-β and tau. Therefore, we compared the intracerebral amyloid and
tau burden
in vivo in a group of super-agers (SA), normal-agers (NA) and patients with mild cognitive impairment (MCI) using PET imaging.
Methods:
Data used for analysis were retrieved from the Alzheimer’s Disease
Neuroimaging Initiative database (http://adni.loni.usc.edu/)
and included three age- and education-matched
groups of 26 SA, 25 NA and 25 MCI patients, all above 80 years of age.
SA were
defined as individuals performing above a
z-score of 1.5 over a four-year period including the time-point of the
PET scan
acquisitions. NA presented average (0.5 <
z-score > 1.5) and MCI patients below average (z-score < 0)
cognitive performance
in this time period. In addition, 18 younger
cognitively-normal, amyloid-negative controls (YA; M(Age)= 63.2 years)
were included
as reference group. [18F]AV-1451 and [18F]AV-45
scans were available for all individuals. The PET scans were
pre-processed
including normalization to MNI space, smoothing
and intensity standardization to the cerebellum. For statistical
analysis,
voxel-wise comparisons (p < .001, uncorr.)
and a region-of-interest (ROI) analysis (p < .05) were conducted,
comparing tau
and amyloid burden between the four groups,
respectively. Moreover, a logistic regression was performed to identify
genetic
and pathophysiological factors best predicting
the different aging processes.
Results: No significant differences between SA and YA were observed in terms of in vivo
tau and amyloid burden. The NA group exhibited higher tau burden in
inferior temporal and precuneal areas and no significant
differences in amyloid burden, when compared to
the YA group. The MCI patients showed both high amyloid and tau
pathology
burden. Differences in amyloid burden predicted
NA from MCI, whereas lower tau burden and lower polygenic risk predicted
SA
from MCI.
Conclusions:
The phenomenon of super-aging appears to be associated with the
resistance to tau and amyloid pathology, which likely permits
maintenance of cognitive performance despite
advanced age. In turn, differences between normal aging and MCI appear
to be
driven by the level of amyloid burden. These
results motivate further research to determine responsible resistance
factors,
which may also inspire the development of novel
treatment concepts.
But is this the correct path to go down or should tau proteins be addressed? Is this just cleaning up existing plaque but not addressing new plaque being generated by tau? Cause and effect once again.
Aducanumab, an antibody developed by the University of Zurich, has
been shown to trigger a meaningful reduction of harmful beta-amyloid
plaques in patients with early-stage Alzheimer's disease. These protein
deposits in the brain are a classic sign of Alzheimer's disease and
contribute to the progressive degeneration of brain cells. The
researchers furthermore demonstrated in an early stage clinical study
that, after one year of treatment with Aducanumab, cognitive decline
could be significantly slowed in antibody-treated patients as opposed to
the placebo group.
Although the causes of Alzheimer's disease are still unknown, it is
clear that the disease commences with progressive amyloid deposition in
the brains of affected persons between ten and fifteen years before the
emergence of initial clinical symptoms such as memory loss. Researchers
have now been able to show that Aducanumab, a human monoclonal antibody,
selectively binds brain amyloid plaques, thus enabling microglial cells
to remove the plaques. A one-year treatment with the antibody, as part
of a phase Ib study, resulted in almost complete clearance of the brain
amyloid plaques in the study group patients. The results, which were
realized by researchers at UZH together with the biotech company
“Biogen” and the UZH spin-off “Neurimmune,” have been published in the
renowned science journal “Nature.”
Reduction of brain amyloid plaque is dependent on treatment duration and dosage
“The results of this clinical study make us optimistic that we can
potentially make a great step forward in treating Alzheimer's disease,”
says Roger M. Nitsch, professor at the Institute for Regenerative
Medicine at UZH. “The effect of the antibody is very impressive. And the
outcome is dependent on the dosage and length of treatment.” After one
year of treatment, practically no beta-amyloid plaques could be detected
in the patients who received the highest dose of the antibody.
The antibody was developed with the help of a technology platform
from “Neurimmune.” Using blood collected from elderly persons aged up to
one hundred and demonstrating no cognitive impairment, the researchers
isolated precisely those immune cells whose antibodies are able to
identify toxic beta-amyloid plaques but not the amyloid precursor
protein that is present throughout the human body and that presumably
plays an important role in the growth of nerve cells. The good safety
profile of Aducanumab in patients may well be attributed to the
antibody’s specific capacity to bond with the abnormally folded
beta-amyloid protein fragment as well as the fact that the antibody is
of human origin.
Investigational treatment also curbs cognitive decline
165 patients with early-stage Alzheimer's disease were treated in the
phase 1b clinical trial. Although not initially planned as a primary
study objective, the good results encouraged researchers to additionally
investigate how the treatment affected the symptoms of disease. This
was evaluated via standardized questionnaires to assess the cognitive
abilities and everyday activities of the patients. “Aducanumab also
showed positive effects on clinical symptoms," is how Nitsch sums up the
findings. “While patients in the placebo group exhibited significant
cognitive decline, cognitive ability remained distinctly more stable in
patients receiving the antibody.”
Some of the trial participants temporarily suffered from
amyloid-related imaging abnormality (ARIA), an adverse effect that can
be detected via magnetic resonance imaging. In a minority of cases, this
was accompanied by temporary mild to moderate headaches. The UZH
researchers believe that ARIA is a measurable biological effect of
amyloid clearance.
The promising effects of Aducanumab are currently being investigated
in two large phase three clinical studies to further evaluate safety and
efficacy. Involving over 300 centers in 20 countries throughout North
America, Europe, and Asia, these studies are evaluating the
effectiveness and safety of the antibody on a total of 2,700 patients
with early-stage Alzheimer's disease. http://www.media.uzh.ch/en/Press-Releases/2016/alzheimer-aducanumab.html
Full bibliographic informationJeff
Sevigny, Ping Chiao, Thierry Bussière, Paul H. Weinreb, Leslie
Williams, Marcel Maier, Robert Dunstan, Stephen Salloway, Tianle Chen,
Yan Ling, John O’Gorman, Fang Qian, Mahin Arastu, Mingwei Li, Sowmya
Chollate, Melanie S. Brennan, Omar Quintero-Monzon, Robert H. Scannevin,
H. Moore Arnold, Thomas Engber, Kenneth Rhodes, James Ferrero, Yaming
Hang, Alvydas Mikulskis, Jan Grimm, Christoph Hock, Roger M. Nitsch
& Alfred Sandrock. The antibody aducanumab reduces Aβ plaques in Alzheimer’s disease. Nature. September 1, 2016. doi:10.1038/nature19323
What else is your doctor using to treat this? You'll have to ask what is inside the microbubbles. http://www.alphagalileo.org/ViewItem.aspx?ItemId=150641&CultureCode=en
Queensland scientists have found that non-invasive ultrasound
technology can be used to treat Alzheimer’s disease and restore memory.
University of Queensland researchers discovered that the innovative
drug-free approach breaks apart the neurotoxic amyloid plaques that
result in memory loss and cognitive decline.
Welcoming the findings today at UQ’s Queensland Brain Institute,
Queensland Premier Annastacia Palaszczuk said they could have a wide
impact for the community.
“The Government’s $9 million investment into this technology was to
drive discoveries into clinics, and today’s announcement indicates that
together with the Queensland Brain Institute, it was a worthwhile
investment,” Ms Palaszczuk said.
“I want my Government to encourage more of this type of innovative research.
“Our Advance Queensland initiative aims to increase research and
discoveries like this and to put this state’s research at the forefront
internationally by supporting local researchers and helping to keep them
in Queensland.
“These exciting findings will hopefully be of benefit to all Australians in the future.”
QBI Founding Director Professor Perry Bartlett said the discovery – a
result of ‘game-changing’ work performed at the Queensland Brain
Institute’s Clem Jones Centre for Ageing Dementia Research – was made
possible through the support of the State and Federal Governments and
philanthropic support led by the Clem Jones Foundation.
“The
farsighted investment of government and philanthropic partners has
allowed us to build the research excellence and capacity required to
make major discoveries such as this,” Professor Perry Bartlett said.
“I believe the work opens up an entirely novel avenue for future therapeutic treatment.”
Clem Jones Centre for Ageing Dementia Research director Professor
Jürgen Götz said the new treatment method could revolutionise
Alzheimer’s treatment by restoring memory.
“We’re extremely excited by this innovation of treating Alzheimer’s without using drug therapeutics,” Professor Götz said.
“The ultrasound waves oscillate tremendously quickly, activating
microglial cells that digest and remove the amyloid plaques that destroy
brain synapses.
“The word ‘breakthrough’ is often mis-used, but in this case I think
this really does fundamentally change our understanding of how to treat
this disease, and I foresee a great future for this approach.”
Alzheimer’s affects more than two-thirds of dementia patients, and approximately a quarter of a million Australians.
The total number of dementia cases in Australia is expected to rise to 900,000 by 2050.
“With an ageing population placing an increasing burden on the health
system, an important factor is cost, and other potential drug
treatments using antibodies will be expensive,” Professor Götz said.
“In contrast, this method uses relatively inexpensive ultrasound and
microbubble technology which is non-invasive and appears highly
effective.
The approach is able to temporarily open the blood-brain barrier,
activating mechanisms that clear toxic protein clumps and restoring
memory functions.
“With our approach the blood-brain barrier’s opening is only
temporary for a few hours, so it quickly restores its protective role,”
Professor Götz said.
Research has been conducted using mice with an Alzheimer’s model,
with the next step being to scale the research in higher animal models
ahead of human clinical trials, which are at least two years away.
“This treatment restored memory function to the same level of normal healthy mice,” Professor Götz said.
“We’re also working on seeing whether this method clears toxic
protein aggregates in neurodegenerative diseases other than Alzheimer’s
and whether this also restores executive functions, including
decision-making and motor control.”
Findings of the research, “Scanning ultrasound efficiently removes
amyloid-β and restores memory in an Alzheimer's model”, are published in
the journal Science Translational Medicine.
Media: Mikaeli Costello, +61 401 580 685 or
mikaeli.costello@uq.edu.au; Professor Jürgen Götz, +61 7 3346 6329,
j.goetz@uq.edu.au. http://stm.sciencemag.org/content/7/278/278ra3
It
is one of the big scientific mysteries of Alzheimer’s disease: Why do
some people whose brains accumulate the plaques and tangles so strongly
associated with Alzheimer’s not develop the disease?
Now,
a series of studies by Harvard scientists suggests a possible answer,
one that could lead to new treatments if confirmed by other research.
The
memory and thinking problems of Alzheimer’s disease and other
dementias, which affect an estimated seven million Americans, may be
related to a failure in the brain’s stress response system, the new
research suggests. If this system is working well, it can protect the
brain from abnormal Alzheimer’s proteins; if it gets derailed, critical
areas of the brain start degenerating.
The rest is at the link behind the NYTimes paywall.
Human neurons are functional over an entire lifetime, yet
the mechanisms that preserve function and protect against
neurodegeneration during ageing are unknown. Here we show that induction
of the repressor element 1-silencing transcription factor (REST; also
known as neuron-restrictive silencer factor, NRSF) is a universal
feature of normal ageing in human cortical and hippocampal neurons. REST
is lost, however, in mild cognitive impairment and Alzheimer’s disease.
Chromatin immunoprecipitation with deep sequencing and expression
analysis show that REST represses genes that promote cell death and
Alzheimer’s disease pathology, and induces the expression of stress
response genes. Moreover, REST potently protects neurons from oxidative
stress and amyloid β-protein toxicity, and conditional deletion of REST
in the mouse brain leads to age-related neurodegeneration. A functional
orthologue of REST, Caenorhabditis elegans SPR-4, also protects
against oxidative stress and amyloid β-protein toxicity. During normal
ageing, REST is induced in part by cell non-autonomous Wnt signalling.
However, in Alzheimer’s disease, frontotemporal dementia and dementia
with Lewy bodies, REST is lost from the nucleus and appears in
autophagosomes together with pathological misfolded proteins. Finally,
REST levels during ageing are closely correlated with cognitive
preservation and longevity. Thus, the activation state of REST may
distinguish neuroprotection from neurodegeneration in the ageing brain.
And look at that, marijuana may reduce the effect of Alzheimers. When the hell is your doctor going to influence the FDA and Congress to allow marijuana to be legalized?
A great post from Neurorexia
Pot’s not the best thing for your memory. Yes, I know there are
functional potheads who enjoy their greens and get also their work done.
Still, it’s hard to ignore the legions of studies that show Δ9-THC
consumption impairs spatial learning and working memory – that is, the
ability to hold several pieces of information in mind and manipulate
them to reach a mental goal.
Welcome to downtown BC and BC Bud! Source: cannabisculture.com
Yet paradoxically, THC may benefit those with Alzheimer’s disease.
Previous research in rats show that the compound breaks down clumps of
disease-causing proteins (called β-amyloid
plagues) by upregulating a “scissor” enzyme that chops them up.
Sweeping out these junk protein plagues decreased the number of dying
neurons in the hippocampus, a brain area crucial for learning and
memory. THC also has powerful anti-oxidant effects and may protect the integrity of mitochondria – the “power plants” of our cells.
So here’s the dilemma: THC may potentially battle dementia, yet it
also naturally impairs memory. In an unexpected turn of events,
scientists from Louisiana State University discovered a key protein that
mediates THC-caused memory loss, and show in mice that you can have
your edibles and eat it too.
