Biosynthetic Grape Derived Compound Prevents Progression of Alzheimer's

This group of researchers found that certain grape seeds extracts, comprised of a complex mixture of naturally occurring polyphenols, were capable of lessening cognitive deterioration and reducing brain neuropathology.

+Alzheimer's Reading Room

Mount Sinai School of Medicine researchers have succeeded in developing a biosynthetic polyphenol that improves cognitive function in mice with Alzheimer's disease (AD). The findings, published in a recent issue of the Journal of Neuroscience, provide insight in determining the feasibility of biosynthetic polyphenols as a possible therapy for AD in humans, a progressive neurodegenerative disease for which there is currently no cure.

Polyphenols, which occur naturally in grapes, fruits, and vegetables, have been shown to prevent the cognitive decline associated with AD in a mouse model, but the molecules are very complex and are extensively metabolized in the body.

This is the first study to determine which specific subfraction of these molecules penetrates the animal brain, and demonstrate that a drug compound similar to polyphenols can exert similar bioactivities.

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Biosynthetic grape-derived compound prevents progression of Alzheimer's disease in mice

A research group led by Giulio Maria Pasinetti, MD, PhD, Saunders Family Professor and Chair in Neurology at Mount Sinai School of Medicine, has been exploring the application of specific grape-derived polyphenols for the treatment of AD. Previously, this group found that certain grape-seeds extracts, comprised of a complex mixture of naturally occurring polyphenols, were capable of lessening cognitive deterioration and reducing brain neuropathology in an animal model of AD, but they did not know how to manipulate the natural extract into a pharmaceutical compound that could be used by the brain.

"My team, along with many members of the scientific community, did not know how we could harness the efficacy of naturally occurring polyphenols in food for treatment of Alzheimer's disease," Dr. Pasinetti said. "We were skeptical that these naturally occurring polyphenols would reach the brain because they are extensively metabolized following ingestion."

The researchers separated the natural occurring polyphenols from grapes, sorted them by size, and administered each for five months through drinking water to mice genetically altered to develop AD, after which they assessed brain neuropathology and cognitive function of the mice. They identified a specific grape polyphenol metabolite that was capable of selectively reaching and accumulating in the brain. This compound reduced the neuropathology of AD in the brain by preventing the accumulation of abnormal proteins in the brain, a hallmark of AD.

Dr. Pasinetti's team analyzed the structure of this polyphenol by nuclear magnetic resonance imaging and recreated it biosynthetically in the laboratory. Dr. Pasinetti and his collaborators discovered that the synthetic polyphenol generated in the laboratory also promoted plasticity and benefits in learning and memory functions in the brains of the mice.

"While this is an exciting development, we have a lot to discover and many years of testing before this agent can be considered in humans," said Dr. Pasinetti. "I look forward to further studying this compound to determine its feasibility as a treatment for Alzheimer's disease."

Dr. Pasinetti is currently exploring the possibility of delivering biosynthetic polyphenols nasally or subcutaneously, thereby preventing them from being metabolized in the liver.

Mount Sinai researchers are supported by a grant from the National Institutes of Health. Dr. Giulio Maria Pasinetti is a named inventor of a pending patent application filed by Mount Sinai School of Medicine (MSSM) related to the study of Alzheimer's disease. In the event the pending or issued patent is licensed, Dr. Pasinetti would be entitled to a share of any proceeds MSSM receives from the licensee.
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About The Mount Sinai Medical Center

The Mount Sinai Medical Center encompasses both The Mount Sinai Hospital and Mount Sinai School of Medicine. The Mount Sinai Hospital, founded in 1852, is a 1,171-bed tertiary- and quaternary-care teaching facility and one of the nation's oldest, largest and most-respected voluntary hospitals.

For more information, visit http://www.mountsinai.org.

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Original content Bob DeMarco, the Alzheimer's Reading Room

Alive Inside Video Goes Viral, Alzheimer's and Music

Music brings out the "More There" in Alzheimer's Patients. New video alerts the public to this phenomena.

By Bob DeMarco
+Alzheimer's Reading Room

On Tuesday, Carole Larkin wrote an article, Music and Memory, An Old Man's Reaction to Hearing "His" Music, that included a video of a man living with dementia who "came alive" as he was listening to music via an Ipod.

Since then the video has gone "viral" on the internet. The video has been watched more than 500,000 times.

I have to admit, I am a bit envious. Too bad the video of Dotty singing, Shine on Harvest Moon, or Alzheimer's Patient Sings With Parrot and Discusses Breakfast didn't blast off on the Internet.

The Music and Memory video took off because a viewer with lots of social influence posted the link to the video on Reddit. This points out how sharing an article can give it a "big life", and allows information to be found by persons all over the world. Hint.

In case you missed it, here is another view of the video, Man In Nursing Home Reacts To Hearing Music From His Era.

We also have a long list of articles about Alzheimer's and Music which you can find below the video.




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• Lifestyle Changes and Music as Alzheimer's Therapy
• The Neuroscience of Music
• Music Boosts Memory in Alzheimer’s, Is this Why the Poop Song Works
• Does Music Unlock Memory in Alzheimer's Sufferers
• Seniors Bring Song, Hope To Alzheimer Patients
• Alzheimer’s and Music: How a Classical Violinist Brought Great Joy to My Demented Romanian Soul Mate
• Music and Alzheimer’s Disease: Using Music to Engage, Comfort and Bring Joy to Your Loved Ones

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Original content +Bob DeMarco , the Alzheimer's Reading Room

Alzheimer's Facility Evicting Patient

An Alzheimer’s care facility served a resident more than food and medicine. The 81-year-old Alzheimer’s patient received eviction papers.

Alzheimer's Reading Room


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Paul Allen Commits $300M to Understanding of How the Brain Works

“As someone who has been touched by the impact of a neurodegenerative disease — my mother has Alzheimer’s — there’s both a fascination in basic research and the hope that we can move things forward.” -- Paul Allen

Alzheimer's Reading Room

Gene Map of the
Brain

"We’re now launching our search for answers to the biggest questions in neuroscience today.

Those answers will help unlock the principles that drive the fundamental functions of the brain.

We are optimistic they will also apply to many diseases and disorders."

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Paul G. Allen Commits $300M to Expand the Allen Institute for Brain Science to Drive Toward a Complete Understanding of How the Brain Works

Institute announces ambitious 10-year plan to tackle the most complex questions in brain science with a continued commitment to open data sharing

The Allen Institute for Brain Science announced today that, given its achievements to date, Paul G. Allen has committed an additional $300 million to the Institute to significantly expand its scientific programs. Bringing his total commitment to date to $500 million, Allen has charged the Institute with tackling some of the most fundamental and complex questions in brain science today.

The answers to these questions are essential for achieving a complete understanding of how the brain works, what goes wrong in brain-related diseases and disorders, and how best to treat them.

"The accomplishments of the Institute have been truly remarkable," said Paul G. Allen. "With its disciplined, mission-focused approach, the Institute has successfully tackled big-science projects, delivering tangible results that are helping to advance brain research around the world every day. I am excited to expand the scale and scope of the Institute's efforts, and I look forward to seeing what we will accomplish in the future."

Allen's significant new contribution will support the first four years of an ambitious 10-year plan developed by the Allen Institute for Brain Science. The plan calls for a doubling of the Institute's staff to launch three new and complementary scientific initiatives that address critical questions that are central to understanding how the brain works:

• How does the brain store, encode and process information?
• What are the cellular building blocks that underlie all brain function, and are often targets of disease?
• How do those cells develop, and then create the circuits that drive behavior, thought and brain dysfunction?

These three complementary initiatives are designed to yield knowledge of fundamental principles governing brain function, publicly sharable data, and new tools and technologies that will further accelerate progress across the global research community.

"Paul Allen's generosity and bold vision have allowed us to build a unique organization and advance brain research in ways that wouldn't be possible otherwise," said Allan Jones, Ph.D., chief executive officer of the Allen Institute for Brain Science. "This new funding enables us to apply our structured, industrial-scale approach to science to tackle increasingly complex questions about how the brain works—questions that must be answered if we are to understand and treat autism, Alzheimer's disease, depression, traumatic brain injury and the myriad other brain-related diseases and disorders that affect all of us either directly or indirectly."

Expansion

To support the new initiatives, the Allen Institute will expand significantly, with plans to double its current staff to more than 350 employees over the next four years. Hiring has begun across all three initiatives. These programs require a team of leading minds at all levels and from across different disciplines to cross-talk and pool their expertise, working toward common goals.

The Allen Institute has already begun to assemble a powerhouse of noted scientific leaders who will collaborate closely and drive creative discovery, innovation and productivity to achieve the goals of the new initiatives. Christof Koch, Ph.D., joined the Allen Institute from Caltech in 2011 as chief scientific officer. R. Clay Reid, M.D., Ph.D., from Harvard Medical School and Ricardo Dolmetsch, Ph.D., from Stanford University will start in the coming months.

They join the Allen Institute's senior scientific director of research and development, Hongkui Zeng, Ph.D., who oversees the Allen Mouse Brain Connectivity Atlas project and is already using the Allen Institute's existing public data sets to begin classifying different cell populations. Dr. Reid and Dr. Dolmetsch will contribute their respective expertise in neural coding and cell networks to a multidisciplinary conversation with Dr. Zeng and Dr. Koch, who is well known for integrating results from different neuroscientific disciplines to understand the complex computations and functions of the brain.

"The Allen Institute's groundbreaking approach—the way that it conducts 'big science' in an 'open science' fashion—has been a game changer in neuroscience," said Susumu Tonegawa, Ph.D., Nobel Laureate and director of the RIKEN-MIT Center for Neural Circuit Genetics.

"From the accomplishment of the mouse and human brain atlases to this new work in the areas of neural coding and cell circuitry, the Allen Institute is making it possible for the world's scientists to carve inroads in understanding and treating human brain impairments that otherwise would be decades away."

Paul Allen launched the Allen Institute for Brain Science with a seed contribution of $100 million, and based on the successful completion and impact of the Allen Mouse Brain Atlas and other early initiatives, has since contributed an additional $100 million. The $300 million commitment announced today brings Allen's cumulative investment to $500 million, making it one of the largest philanthropic commitments ever to fund neuroscience research.

Bolstered by new funding and new scientific talent, the Allen Institute for Brain Science is further pushing the frontiers of neuroscience with new initiatives and historic aims to accelerate understanding of the human brain in health and disease.

Impact

The Allen Institute's work is used regularly by scientists around the world and has been recognized for its significant impact on brain research, garnering awards from the Society for Neuroscience, the American Academy of Neurology, Time magazine and others.

A pioneer in bringing the "big science" approach to the study of the brain, the Allen Institute has been driving research forward since 2003 by systematically generating massive data sets—comprising a total of 1.3 petabytes to date—and translating them into online public resources.

These resources, all openly available via the Allen Brain Atlas data portal at www.brain-map.org free of charge, have become essential resources for scientists around the globe—from graduate students to large-scale commercial labs.

All together, the Allen Institute's online public resources receive approximately 50,000 visits each month, representing researchers from universities, biotechnology and pharmaceutical companies, government laboratories and other research organizations across about 70 countries worldwide.

These unprecedented data stores and online tools empower scientists to save time—shaving days to months to years off of their research programs—and to make groundbreaking discoveries about brain disease and disorders, helping to ultimately deliver better treatment options sooner.

Researchers studying every facet of normal brain function and disease, from learning, cognition, hearing and development to stroke, Alzheimer's, obesity, schizophrenia, autism, and more, regularly use and cite Allen Institute resources in their research.

Allen Institute for Brain Science



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High Cholesterol Levels in Your 40s May Raise the Chance of Developing Alzheimer's disease

The study found people with total cholesterol levels between 249 and 500 milligrams were one-and-a-half times more likely to develop Alzheimer's disease than those people with cholesterol levels of less than 198 milligrams.

High cholesterol levels in your 40s may raise the chance of developing Alzheimer's disease decades later, according to a study underscoring the importance of health factors in middle age on risk for the brain ailment.

The study involving 9,752 people in northern California found that those with high cholesterol levels between ages 40 and 45 were about 50 percent more likely than those with low cholesterol levels to later develop Alzheimer's disease.

The findings were presented on Wednesday at a meeting of the American Academy of Neurology in Chicago.


"Alzheimer's disease does not happen overnight," Dr. Alina Solomon of the University of Kuopio in Finland, who helped lead the study, said in a telephone interview.

"Alzheimer's disease has a very long preclinical phase — a silent phase — when you don't see any signs of the disease, but the disease is there. The pathological changes in the brain can sometimes develop over decades."

The study found people with total cholesterol levels between 249 and 500 milligrams were one-and-a-half times more likely to develop Alzheimer's disease than those people with cholesterol levels of less than 198 milligrams. People with total cholesterol levels of 221 to 248 milligrams were more than one-and-a-quarter times more likely to develop Alzheimer's disease.

Alzheimer's disease is the most common form of dementia among older people, and researchers have been working to understand its causes and risk factors.

The findings come just weeks after another study showed that having a big belly in middle age may greatly increase one's risk of later developing Alzheimer's disease or another form of dementia.

Rachel Whitmer of the Kaiser Permanente Division of Research in Oakland, California who led that study also was involved in the new one on cholesterol levels.

"Cholesterol is just one piece of the puzzle. There are other risk factors like hypertension and obesity. The more risk factors you have, the higher the risk gets," Solomon said.

Solomon said previous research had looked at the issue of high cholesterol levels in middle age as a risk factor for later development of dementia, but did not focus specifically on Alzheimer's disease.

The people in the new study underwent detailed health evaluations between 1964 and 1973 when they were ages 40 to 45, including blood cholesterol measurements. The researchers then looked at the cholesterol measurements of the 504 people in the study who developed Alzheimer's disease decades later.

High levels of cholesterol — a waxy, fat-like substance that occurs naturally in the body — in the blood can raise one's risk of heart disease. Physical inactivity, obesity and a fatty diet can contribute to high cholesterol.

"The association between cholesterol and cardiovascular disease is well known. What we know now is that minding heart health may protect your brain as well," Solomon said.

Exercise and eating more fruits and vegetables can lower cholesterol, and there are cholesterol-lowering drugs as well.

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Bob DeMarco is the Founder of the Alzheimer's Reading Room and an Alzheimer's caregiver. The ARR knowledge base contains more than 5,000 articles with more than 399,100 links on the Internet. Bob lives in Delray Beach, FL.

Original content Bob DeMarco, the Alzheimer's Reading Room

Eight Types of Dementia Defined

Dementia is a clinical syndrome of loss or decline in memory and other cognitive abilities. It is caused by various diseases and conditions that result in damaged brain cells.

Alzheimer’s disease is the most common cause of dementia.

This section provides information about the definition of dementia, the characteristics of specific types of dementia and the symptoms, risk factors for and treatment of Alzheimer’s disease.

Dementia: Definition and Specific Types

Dementia is a clinical syndrome of loss or decline in memory and other cognitive abilities. It is caused by various diseases and conditions that result in damaged brain cells. To be classified as dementia, the syndrome must meet the following criteria:

• It must include decline in memory and in at least one of the following cognitive abilities:

1. Ability to generate coherent speech and understand spoken or written language;

2. Ability to recognize or identify objects, assuming intact sensory function;

3. Ability to execute motor activities, assuming intact motor abilities, sensory function and comprehension
of the required task; and

4. Ability to think abstractly, make sound judgments and plan and carry out complex tasks.


• The decline in cognitive abilities must be severe enough to interfere with daily life.
Diff erent types of dementia have been associated with distinct symptom patterns and distinguishing microscopic brain abnormalities. Increasing evidence from long-term epidemiological observation and autopsy studies suggests that many people have microscopic brain abnormalities associated with more than one type of dementia. The symptoms of diff erent types of dementia also overlap and can be further complicated by coexisting medical
conditions.

Table 1 provides information about the most common types of dementia.

Table 1: Common Types of Dementia and Their Typical Characteristics

Type of Dementia Characteristics

Alzheimer’s disease. Most common type of dementia; accounts for 60 to 80 percent of cases.

Difficulty remembering names and recent events is often an early clinical
symptom; later symptoms include impaired judgment, disorientation, confusion,
behavior changes and trouble speaking, swallowing and walking.

Hallmark abnormalities are deposits of the protein fragment beta-amyloid
(plaques) and twisted strands of the protein tau (tangles).

Vascular dementia. Considered the second-most-common type of dementia.

Impairment is caused by decreased blood fl ow to parts of the brain, often due
to a series of small strokes that block arteries.

Symptoms often overlap with those of Alzheimer’s, although memory may not
be as seriously aff ected.

Mixed dementia. Characterized by the presence of the hallmark abnormalities of Alzheimer’s
and another type of dementia, most commonly vascular dementia, but also
other types, such as dementia with Lewy bodies, frontotemporal dementia and
normal pressure hydrocephalus.

Dementia with Lewy bodies. Pattern of decline may be similar to Alzheimer’s, including problems with memory, judgment and behavior changes.

Alertness and severity of cognitive symptoms may fluctuate daily.

Visual hallucinations, muscle rigidity and tremors are common.

Hallmarks include Lewy bodies (abnormal deposits of the protein alphasynuclein)
that form inside nerve cells in the brain.


Parkinson’s disease. Many people who have Parkinson’s disease develop dementia in the later stages of the disease.

The hallmark abnormality is Lewy bodies (abnormal deposits of the protein
alpha-synuclein) that form inside nerve cells in the brain.

Frontotemporal dementia. Involves damage to brain cells, especially in the front and side regions
of the brain.

Typical symptoms include changes in personality and behavior and diffi culty
with language.

No distinguishing microscopic abnormality is linked to all cases.

Pick’s disease, characterized by “Pick’s bodies,” is one type of frontotemporal
dementia.

Creutzfeldt-Jakob disease. Rapidly fatal disorder that impairs memory and coordination and causes behavior changes.

“Variant Creutzfeldt-Jakob disease” is believed to be caused by consumption of
products from cattle affected by “mad cow disease.”

Caused by the misfolding of prion protein throughout the brain.

Normal pressure hydrocephalus. Caused by the buildup of fl uid in the brain.
Symptoms include difficulty walking, memory loss and inability to control urine.

Can sometimes be corrected with surgical installation of a shunt in the brain to
drain excess fluid.

Mild cognitive impairment is a condition in which a person has problems with memory, language or another essential cognitive function that are severe enough to be noticeable to others and show up on tests, but not severe enough to interfere with daily life. Some people with mild cognitive impairment go on to develop dementia. For others, the symptoms of mild cognitive impairment do not progress to dementia, and some people who have mild cognitive impairment at one point in time later revert to normal cognitive status.

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Bob De Marco
Alzheimer's Reading Room

Original content Bob DeMarco, the Alzheimer's Reading Room