Still, over the past couple of years, one of the latest entries to the class of anti-amyloid immunotherapies has lived up to some of the promise first seen in animal
studies of amyloid clearance.
Not exact matches
«Because brain cells release
amyloid beta during activity, we think if the brain cells can't rest the way they're supposed to and get that deep sleep, they produce a relative excess
of amyloid,» Dr. Yo - El Ju
of Washington University, an author
of that
study, told Reuters.
For example, Eli Lilly & Co. (NYSE: LLY) has a phase 3
study of solanezumab under way in mild to moderate Alzheimer's disease patients that may slow disease progression by breaking up
amyloid plaque buildups thought to be a major cause
of the disease.
It offers cardio protection, it helps lower bad cholesterol, it may help prevent the progression
of multiple sclerosis, it has the ability to regenerate brain cells after a stroke, it has the ability to cross the blood - brain barrier to potentially ward off Alzheimer's disease, apparently it's good at wiping
amyloid plaque from the brain (which
studies haves linked to Alzheimer's), it may help to prevent certain types
of cancer, and
studies have shown that it inhibits cancer cell growth and metastases (meaning it keeps cancer from spreading).
The title
of the
study is «Coconut Oil Attenuates the Effects
of Amyloid - on Cortical Neurons In Vitro.»
A Canadian
study published this year around the same time titled «Coconut oil protects cortical neurons from
amyloid beta toxicity by enhancing signaling
of cell survival pathways» observed that coconut oil and its medium chain fatty acids (MCFAs) protect against
amyloid beta (Aβ) induced neurotoxicity in primary rat cortical neurons.
Senior
study author Katsuhiko Yanagisawa, director general
of the National Center for Geriatrics and Gerontology in Japan, is convinced that enough
amyloid penetrates the blood — brain barrier to make its way into the bloodstream to be a useful measure
of cognitive function.
Within a couple
of years, interest in ApoE had dwindled as researchers flocked to
study amyloid - β.
Yanagisawa and colleagues are now extending and expanding their
study in hopes
of bringing an
amyloid blood test closer to routine clinical use.
Imaging
studies have shown that the brains
of high - risk individuals look and behave differently from controls decades before the onset
of Alzheimer's, and long before they start to accumulate
amyloid - β or lose grey matter.
In a
study published online June 21 in the Annals
of Clinical and Translational Neurology, the researchers show that the consumption
of extra-virgin olive oil protects memory and learning ability and reduces the formation
of amyloid - beta plaques and neurofibrillary tangles in the brain — classic markers
of Alzheimer's disease.
The idea for Smith's
study was inspired by the work
of co-author Alena Savonenko, M.D., Ph.D., associate professor
of pathology, and her colleagues who showed that loss
of serotonin neurons was associated with more protein clumps, or
amyloid, in mouse brain.
The Loyola
study is titled, «Endocytic vesicle rupture is a conserved mechanism
of cellular invasion by
amyloid proteins.»
Recent
studies in those with an inherited form
of early Alzheimer's detected the presence
of rogue
amyloid proteins up to two decades before symptoms emerged, suggesting that we're intervening too late, when the damage is irreparable.
A new
study suggests an association between elevated
amyloid beta levels and the worsening
of anxiety symptoms.
Past
studies have suggested depression and other neuropsychiatric symptoms may be predictors
of AD's progression during its «preclinical» phase, during which time brain deposits
of fibrillar
amyloid and pathological tau accumulate in a patient's brain.
One
study, called A4 (the anti-
amyloid treatment in asymptomatic Alzheimer's trial), will test solanezumab in 1,000 cognitively normal people age 65 to 85, who have abnormally high levels
of amyloid proteins.
In 2013 another
study will focus on a family in Colombia that carries one
of these rogue genes, treating them with the
amyloid - fighting drug Crenezumab.
We see manifold applications, such as
studies of conformational changes in
amyloid structures on the molecular level, the mapping
of nanoscale protein modifications in biomedical tissue or the label - free mapping
of membrane proteins.
This
study was the first major Alzheimer's clinical trial to require molecular evidence
of amyloid deposition in the brain for enrollment.
In the current
study, a collaborative team
of researchers at the Gladstone Institute and the Baylor College
of Medicine in Houston, created a strain
of mice that overproduces a precursor
of Aβ known as
amyloid precursor protein.
The new
study is a «proof
of concept» in animals that ß
amyloid does indeed protect against pathogens, Tanzi says.
ß -
amyloid deposits can damage many organs besides the brain, including the heart, liver, and kidneys, says neuroscientist Rudolph Tanzi
of Massachusetts General Hospital (MGH) in Boston, a leader
of the new
study.
«Our
study shows that both higher levels
of HDL — good — and lower levels
of LDL — bad — cholesterol in the bloodstream are associated with lower levels
of amyloid plaque deposits in the brain,» said Bruce Reed, lead
study author and associate director
of the UC Davis Alzheimer's Disease Center.
The high prevalence
of OSA the
study found in these cognitively normal elderly participants and the link between OSA and
amyloid burden in these very early stages
of AD pathology, the researchers believe, suggest the CPAP, dental appliances, positional therapy and other treatments for sleep apnea could delay cognitive impairment and dementia in many older adults.
A
study headed by researchers at the Institute for Research in Biomedicine (IRB Barcelona) and the Institut Européen de Chimie et Biologie (IECB) in France proposes that the presence
of two beta -
amyloid molecules bound together (beta -
amyloid dimers) could provide a new biomarker for AD.
«Several
studies have suggested that sleep disturbances might contribute to
amyloid deposits and accelerate cognitive decline in those at risk for AD,» said Ricardo S. Osorio, MD, senior
study author and assistant professor
of psychiatry at New York University School
of Medicine.
«Activation
of these cell receptors appear to prevent brain cells from cleaning out the trash — the toxic buildup
of proteins, such as alpha - synuclein, tau and
amyloid, common in neurodegenerative diseases,» says the
study's senior author, neurologist Charbel Moussa, MBBS, PhD, director
of Georgetown's Laboratory for Dementia and Parkinsonism, and scientific and clinical research director
of the GUMC Translational Neurotherapeutics Program.
Amyloid — an abnormal protein whose accumulation in the brain is a hallmark
of Alzheimer's disease — starts accumulating inside neurons
of people as young as 20, a much younger age than scientists ever imagined, reports a surprising new Northwestern Medicine
study.
But with the human cells, Young - Pearse and her team, including postdoctoral fellow and
study first author, Christina Muratore, could demonstrate that preventing
amyloid - beta imbalances reduced levels
of distorted tau.
Various
studies have linked Alzheimer's disease to the accumulation
of two particular proteins in the brain called
amyloid - beta and tau.
«This new
study extends those original mechanistic findings to the
amyloid pathway and preservation
of cellular and synaptic connections.
A new
study appearing in the Journal
of Neuroinflammation suggests that the brain's immune system could potentially be harnessed to help clear the
amyloid plaques that are a hallmark
of Alzheimer's disease.
He added that the purpose
of this
study was to investigate the associations between OSA severity and changes in AD biomarkers longitudinally, specifically whether
amyloid deposits increase over time in healthy elderly participants with OSA.
The
amyloid theory has legs, but the new
study could have provided a better demonstration, says James Milner - White at the University
of Glasgow, UK.
«However, we are also
studying the effects
of pazopanib on
amyloid beta to create a better understanding
of how it works and what diseases it could potentially be used to treat.»
«This
study has allowed us to sort out, in mice, which effects
of the different types
of APOE were most important to variation in
amyloid plaque deposition,» says Eloise Hudry, PhD,
of MGH - MIND, lead author
of the Science Translational Medicine report.
«This research confirms earlier observations that, when activated to fight inflammation, the brain's immune system plays a role in the removal
of amyloid beta,» said M. Kerry O'Banion, M.D., Ph.D., a professor in the University
of Rochester Department
of Neurobiology and Anatomy, the Del Monte Neuromedicine Institute, and the lead author
of the
study.
The
study noted increased levels
of amyloid beta in a large group
of patients with no hereditary risk gene.
Scientific Paper 124: «Differential contributions
of Amyloid and Tau burden to Neuro - degeneration in Alzheimer's Disease: A multimodal in vivo PET
study.»
Studies in mice specially bred to have features
of the disease found that DHA reduces beta -
amyloid plaques, abnormal protein deposits in the brain that are a hallmark
of Alzheimer's, although a clinical trial
of DHA showed no impact on people with mild to moderate Alzheimer's disease.
Studies suggest that adults with high brain
amyloid have elevated risk for Alzheimer's and stand the best chance
of benefiting from treatments should they become available.
The
study also confirmed similarities between Type 2 diabetes and Alzheimer's and other neurodegenerative diseases that are marked by an accumulation
of toxic forms
of amyloid proteins, she said.
«This
study provides evidence that there is plasticity or compensation ability in the aging brain that appears to be beneficial, even in the face
of beta -
amyloid accumulation,» said
study principal investigator Dr. William Jagust, a professor with joint appointments at UC Berkeley's Helen Wills Neuroscience Institute, the School
of Public Health and Lawrence Berkeley National Laboratory.
For this
study, 10 subjects with Alzheimer's underwent PET following the injection
of three radiotracers: fluorine - 18 fluorodeoxyglucose (F - 18 FDG), which images regional metabolic activity; carbon - 11 Pittsburgh compound B (C - 11 PiB), which has an affinity for
amyloid plaques; and F - 18 AV - 1451, an emerging imaging agent that binds to tau in the brain.
In fact, in another
study published last year, National Institute on Aging (NIA) researchers discovered that people with what's called a CR1 gene variant — the presence
of which heightens Alzheimer's disease risk — had much lower levels
of amyloid protein compared with those without the mutant gene.
«The body produces a lot
of amyloids after an injury, so in some circumstances, they may be performing a guardian function,» says
study co-author and Stanford neurologist Lawrence Steinman.
In the new
study, Ances and colleagues used one
of these tags and an
amyloid - binding one to analyze deposits
of both proteins in 10 people with mild AD and 36 healthy adults.
That
study was the lab's first attempt to model the energy landscape
of amyloid aggregation, which has been implicated in Alzheimer's disease.
Now, a new imaging
study of 10 people with mild AD suggests that tau deposits — not
amyloid — are closely linked to symptoms such as memory loss and dementia.