Compounds in the spice shown to prevent “tangles” in brain cells that are typical of disease.

Roshni George (left) and Donald Graves of UC Santa Barbara have found that certain compounds in cinnamon can prevent the protein "tangles" that occur in the brain cell with Alzheimer's.

Cinnamon: Can the red-brown spice with the unmistakable fragrance and variety of uses offer an important benefit? The common baking spice might hold the key to delaying the onset of –– or warding off –– the effects of Alzheimer’s disease.

That is, according to Roshni George and Donald Graves, scientists at UC Santa Barbara. The results of their study, “Interaction of Cinnamaldehyde and Epicatechin with Tau: Implications of Beneficial Effects in Modulating Alzheimer’s Disease Pathogenesis,” appears in the online early edition of the Journal of Alzheimer’s Disease, and in the upcoming Volume 36, issue 1 print edition.

Alzheimer’s disease is the most common form of dementia, a neurodegenerative disease that progressively worsens over time as it kills brain cells. No cure has yet been found, nor has the major cause of Alzheimer’s been identified.

However, two compounds found in cinnamon –– cinnamaldehyde and epicatechin –– are showing some promise in the effort to fight the disease. According to George and Graves, the compounds have been shown to prevent the development of the filamentous “tangles” found in the brain cells that characterize Alzheimer’s.

Read more

Center brings together many disciplines to respond to President Obama’s “grand challenge.”

(From left) Nick Spitzer, Ralph Greenspan and Terry Sejnowski.

Responding to President Barack Obama’s “grand challenge” to chart the function of the human brain in unprecedented detail, UC San Diego has established the Center for Brain Activity Mapping (CBAM). The new center, under the aegis of the interdisciplinary Kavli Institute for Brain and Mind at UC San Diego, will tackle the technological and biological challenge of developing a new generation of tools to enable recording of neuronal activity throughout the brain. It will also conduct brain-mapping experiments and analyze the collected data.

Ralph Greenspan – one of the original architects of a visionary proposal that eventually led to the national BRAIN Initiative launched by President Obama in April – has been named CBAM’s founding director.

UC San Diego Chancellor Pradeep K. Khosla, who attended Obama’s unveiling of the BRAIN Initiative, said: “I am pleased to announce the launch of the Center for Brain Activity Mapping. This new center will require the type of in-depth and impactful research that we are so good at producing at UC San Diego. We have strengths here on our campus and the Torrey Pines Mesa, both in breadth of talent and in the scientific openness to collaborate across disciplines, that few others can offer the project.”

Greenspan, who also serves as associate director of the Kavli Institute for Brain and Mind at UC San Diego, said CBAM will focus on developing new technologies necessary for global brain-mapping at the resolution level of single cells and the timescale of a millisecond, participate in brain mapping experiments, and develop the necessary support mechanisms for handling and analyzing the enormous datasets that such efforts will produce.

Brain-mapping discoveries made by CBAM may shed light on such brain disorders as autism, traumatic brain injury and Alzheimer’s – and could potentially point the way to new treatments, Greenspan said. The technologies developed and advances in understanding brain networks will also likely have industrial applications outside of medicine, he said.

The new center will bring together researchers from neuroscience (including cognitive science, psychology, neurology and psychiatry), engineering, nanoscience, radiology, chemistry, physics, computer science and mathematics.

“An essential component of the center will be its close relationships with other San Diego research institutions and with industrial partners in the region’s high-tech and biotech clusters,” said Nick Spitzer, distinguished professor of neurobiology and director of the Kavli Institute for Brain and Mind at UC San Diego.

Read more

Related link:
UC researchers part of Obama initiative to map the brain

Fictional monsters could help educate public about rabies, Alzheimer’s.

Zombies have inspired countless horror films and graphic novels, but the fictional monsters have recently been used for a loftier goal: public health awareness. UC Irvine lecturer/researcher Brandon Brown, Ph.D., and public health grad student Melissa Nasiruddin published a paper (and podcast) in the journal Emerging Infectious Diseases that advocates using zombies to educate the moviegoing masses about re-emerging infectious diseases such as rabies and neurological conditions such as Alzheimer’s and Parkinson’s.

“Rabies isn’t a problem in the United States, but China and Indonesia have recently had outbreaks of the disease,” Nasiruddin said. Rabies and zombiism are both transmitted through bites, and both cause foaming at the mouth.

Zombies and people with Parkinson’s disease both experience muscle rigidity, tremors, a shuffling gait and slowness. If conflating public health and zombies sounds familiar, it’s probably because of the Centers for Disease Control & Prevention’s successful campaign linking reports of zombie infestations to disaster readiness. “If you can prepare for a fictional zombie apocalypse, you can prepare for the outbreak of any disease or global pandemic,” Brown said.

Read more

Brain imaging, stroke risk assessment detect the signs before symptoms appear.

Brain scan of patient with mild cognitive impairment (MCI)

UCLA researchers have used a brain-imaging tool and stroke risk assessment to identify signs of cognitive decline early on in individuals who don’t yet show symptoms of dementia.

The connection between stroke risk and cognitive decline has been well established by previous research. Individuals with higher stroke risk, as measured by factors like high blood pressure, have traditionally performed worse on tests of memory, attention and abstract reasoning.

The current small study demonstrated that not only stroke risk, but also the burden of plaques and tangles, as measured by a UCLA brain scan, may influence cognitive decline.

The imaging tool used in the study was developed at UCLA and reveals early evidence of amyloid beta “plaques” and neurofibrillary tau “tangles” in the brain — the hallmarks of Alzheimer’s disease.

The study, published in the April issue of the Journal of Alzheimer’s Disease, demonstrates that taking both stroke risk and the burden of plaques and tangles into accout may offer a more powerful assessment of factors determining how people are doing now and will do in the future.

“The findings reinforce the importance of managing stroke risk factors to prevent cognitive decline even before clinical symptoms of dementia appear,” said first author David Merrill, an assistant clinical professor of psychiatry and biobehavioral sciences at the Semel Institute for Neuroscience and Human Behavior at UCLA.

Read more

Project to provide insight on diseases, how we think, learn and remember.

University of California scientists are among the brains behind President Obama’s national initiative to map the human brain.

On April 2, Obama proposed an initial $100 million investment this year in the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) initiative. The goal is to help researchers find new ways to treat, cure and prevent brain disorders such as Alzheimer’s disease, epilepsy and traumatic brain injury, according to a White House press release.

The idea to map the brain was proposed last year by a group of leading scientists that included Lawrence Berkeley National Lab Director Paul Alivisatos and Ralph Greenspan, associate director of UC San Diego’s Kavli Institute.

“The Brain Activity Map is a very promising project for developing revolutionary new tools to advance neuroscience and to enable improved understanding of neurological diseases,” Alivisatos said. “It is exciting that the nation will lean forward to make progress in this important area.”

Cornelia “Cori” Bargmann, a former UCSF professor now at Rockefeller University, and William Newsome of Stanford University, will co-chair BRAIN.

BRAIN will combine the efforts of universities, private organizations and federal research agencies, such as the National Institutes of Health, in a massive project to decipher how the brain works.

UC neuroscientists, chemists, computer scientists, physicists and engineers will take part in the effort.

“There is this enormous mystery waiting to be unlocked, and the BRAIN Initiative will change that by giving scientists the tools they need to get a dynamic picture of the brain in action and better understand how we think and how we learn and how we remember,” Obama said. “And that knowledge could be — will be — transformative.”

For more coverage of UC’s role in the BRAIN initiative, view these links:

• UC Berkeley: Campus poised to join Obama’s BRAIN initiative
• Chancellor leads UCLA contingent to White House for announcement of BRAIN initiative
• UC San Diego: Mapping the mind
• Brain research at UC San Diego brings excitement to celebration of former engineering dean
• UCSF: President Obama unveils brain mapping project
• UCTV: UC and the BRAIN initiative

UC Riverside researchers discover sleep mechanism critical to memory consolidation.

Sara Mednick, UC Riverside

A team of sleep researchers led by UC Riverside psychologist Sara C. Mednick has confirmed the mechanism that enables the brain to consolidate memory and found that a commonly prescribed sleep aid enhances the process. Those discoveries could lead to new sleep therapies that will improve memory for aging adults and those with dementia, Alzheimer’s and schizophrenia.

The groundbreaking research appears in a paper, “The Critical Role of Sleep Spindles in Hippocampal-Dependent Memory: A Pharmacology Study,” published in the Journal of Neuroscience.

Earlier research found a correlation between sleep spindles — bursts of brain activity that last for a second or less during a specific stage of sleep — and consolidation of memories that depend on the hippocampus. The hippocampus, part of the cerebral cortex, is important in the consolidation of information from short-term to long-term memory, and spatial navigation. The hippocampus is one of the first regions of the brain damaged by Alzheimer’s disease.

Mednick and her research team demonstrated, for the first time, the critical role that sleep spindles  play in consolidating memory in the hippocampus, and they showed that pharmaceuticals could significantly improve that process, far more than sleep alone.

In addition to Mednick the research team includes:  Elizabeth A. McDevitt, UC San Diego; James K. Walsh, VA San Diego Healthcare System, La Jolla; Erin Wamsley, St. Luke’s Hospital, St. Louis, Mo.; Martin Paulus, Stanford University; Jennifer C. Kanady, Harvard Medical School; and Sean P.A. Drummond, UC Berkeley.

“We found that a very common sleep drug can be used to increase verbal memory,” said Mednick, the lead author of the paper that outlines results of two studies conducted over five years with a $651,999 research grant from the National Institutes of Health. “This is the first study to show you can manipulate sleep to improve memory. It suggests sleep drugs could be a powerful tool to tailor sleep to particular memory disorders.”

Read more

UCLA researchers find signs of disease decades before illness strikes.

Paul Thompson, UCLA

Scientists at UCLA have discovered a new genetic risk factor for Alzheimer’s disease by screening people’s DNA and then using an advanced type of scan to visualize their brains’ connections.

Alzheimer’s disease, the most common cause of dementia in the elderly, erodes these connections, which we rely on to support thinking, emotion and memory. With no known cure for the disease, the 20 million Alzheimer’s sufferers worldwide lack an effective treatment. And we are all at risk: Our chance of developing Alzheimer’s doubles every five years after age 65.

The UCLA researchers discovered a common abnormality in our genetic code that increases the risk of Alzheimer’s. To find the gene, they used a new imaging method that screens the brain’s connections — the wiring, or circuitry, that communicates information. Switching off such Alzheimer’s risk genes (nine of them have been implicated over the last 20 years) could stop the disorder in its tracks or delay its onset by many years.

The research is published in the March 4 online edition of the journal Proceedings of the National Academy of Sciences.

“We found a change in our genetic code that boosts our risk for Alzheimer’s disease,” said the study’s senior author, Paul Thompson, a UCLA professor of neurology and a member of the UCLA Laboratory of Neuro Imaging. “If you have this variant in your DNA, your brain connections are weaker. As you get older, faulty brain connections increase your risk of dementia.”

Read more

UC Davis’ Owen Carmichael will work to develop key biomarkers.

Owen Carmichael, UC Davis

Beginning in midlife, heart disease leads to subtle blood-flow problems in the brain that develop insidiously, gradually damaging neurons and contributing to cognitive decline. Knowledge of clinically silent blood-flow problems in the brain has led to the “healthy heart, healthy mind” hypothesis that preventing or treating heart disease also may help prevent age-associated cognitive decline.

However, the healthy heart, healthy mind hypothesis has been difficult to test because of a lack of validated markers of subtle blood-flow problems in the brains of otherwise healthy elderly adults. Owen Carmichael, associate professor in the UC Davis Department of Neurology, will work to develop such biomarkers through a new two-year, $100,000 grant from the Alzheimer’s Association.

Carmichael and his colleagues will enroll 50 cognitively healthy people who already have received multiple clinical evaluations, cognitive testing and MRIs at the UC Davis Alzheimer’s Disease Center. They will receive an additional MRI scan designed to detect subtle blood-flow disruptions that may develop over time and damage brain tissue. They also will receive PET scans to measure their amyloid burden and determine whether preclinical Alzheimer’s disease is promoting brain injury and cognitive decline concurrent with blood-flow problems. Amyloid beta plaques in the brain have been associated with Alzheimer’s disease.

“We will evaluate the usefulness of our cerebrovascular measurements by examining how they relate to MRI-based measurements of brain injury and cognitive function,” Carmichael said. “Success in this project could lead to the use of these imaging markers for clinical assessment of preclinical cerebrovascular disease and for measuring the effects of cardiovascular treatments on the aging brain.”

Synaptic molecule works differently than thought; may mean new therapeutic targets for treating Alzheimer’s.

Roberto Malinow, UC San Diego

In a pair of new papers, researchers at the UC San Diego School of Medicine and the Royal Netherlands Academy of Arts and Sciences upend a long-held view about the basic functioning of a key receptor molecule involved in signaling between neurons, and describe how a compound linked to Alzheimer’s disease impacts that receptor and weakens synaptic connections between brain cells.

The findings are published in the Feb. 18 early edition of the Proceedings of the National Academy of Sciences.

Long the object of study, the NMDA receptor is located at neuronal synapses – the multitudinous junctions where brain cells trade electrical and chemical messages. In particular, NMDA receptors are ion channels activated by glutamate, a major “excitatory” neurotransmitter associated with cognition, learning and memory.

“NMDA receptors are well known to allow the passage of calcium ions into cells and thereby trigger biochemical signaling,” said principal investigator Roberto Malinow, M.D., Ph.D., professor of neurosciences at UC San Diego School of Medicine.

The new research, however, indicates that NMDA receptors also can operate independent of calcium ions. “It turns upside down a view held for decades regarding how NMDA receptors function,” said Malinow, who holds the Shiley-Marcos Endowed Chair in Alzheimer’s Disease Research in Honor of Dr. Leon Thal (a renowned UC San Diego Alzheimer’s disease researcher who died in a single-engine airplane crash in 2007).

Read more

“The more vascular brain injury the participants had, the worse their memory.”

Bruce Reed, UC Davis

Vascular brain injury from conditions such as high blood pressure and stroke are greater risk factors for cognitive impairment among non-demented older people than is the deposition of the amyloid plaques in the brain that long have been implicated in conditions such as Alzheimer’s disease, a study by researchers at the Alzheimer’s Disease Research Center at UC Davis has found.

Published online early today in JAMA Neurology (formerly Archives of Neurology), the study found that vascular brain injury had by far the greatest influence across a range of cognitive domains, including higher-level thinking and the forgetfulness of mild cognitive decline.

The researchers also sought to determine whether there was a correlation between vascular brain injury and the deposition of beta amyloid (Αβ) plaques, thought to be an early and important marker of Alzheimer’s disease, said Bruce Reed, associate director of the UC Davis Alzheimer’s Disease Research Center in Martinez. They also sought to decipher what effect each has on memory and executive functioning.

“We looked at two questions,” said Reed, professor in the Department of Neurology at UC Davis. “The first question was whether those two pathologies correlate to each other, and the simple answer is ‘no.’ Earlier research, conducted in animals, has suggested that having a stroke causes more beta amyloid deposition in the brain. If that were the case, people who had more vascular brain injury should have higher levels of beta amyloid. We found no evidence to support that.”

“The second,” Reed continued, “was whether higher levels of cerebrovascular disease or amyloid plaques have a greater impact on cognitive function in older, non-demented adults. Half of the study participants had abnormal levels of beta amyloid and half vascular brain injury, or infarcts. It was really very clear that the amyloid had very little effect, but the vascular brain injury had distinctly negative effects.”

“The more vascular brain injury the participants had, the worse their memory and the worse their executive function – their ability to organize and problem solve,” Reed said.

Other study authors include Natalie Marchant of UC Berkeley and the Buck Institute for Research on Aging; Roxana Dhada and William Jagust  of UC Berkeley; Charles DeCarli and Dan Mungas of UC Davis; Stephen Kriger and Micheal Weiner of UC San Francisco and Nerses Sanossian, Wendy Mack and Helena Chui of the University of Southern California.

Read more

UCLA study shows potential for boosting immunity, clearing amyloid plaques.

Milan Fiala, UCLA

A team of academic researchers has pinpointed how vitamin D3 and omega-3 fatty acids may enhance the immune system’s ability to clear the brain of amyloid plaques, one of the hallmarks of Alzheimer’s disease.

In a small pilot study published in today’s (Feb. 5) issue of the Journal of Alzheimer’s Disease, the scientists identified key genes and signaling networks regulated by vitamin D3 and the omega-3 fatty acid DHA (docosahexaenoic acid) that may help control inflammation and improve plaque clearance.

Previous laboratory work by the team helped clarify key mechanisms involved in helping vitamin D3 clear amyloid-beta, the abnormal protein found in the plaque. The new study extends the previous findings with vitamin D3 and highlights the role of omega-3 DHA.

“Our new study sheds further light on a possible role for nutritional substances such as vitamin D3 and omega-3 in boosting immunity to help fight Alzheimer’s,” said study author Dr. Milan Fiala, a researcher at the David Geffen School of Medicine at UCLA.

For the study, scientists drew blood samples from both Alzheimer’s patients and healthy controls, then isolated critical immune cells called macrophages from the blood. Macrophages are responsible for gobbling up amyloid-beta and other waste products in the brain and body.

Read more

Recipients include UC Berkeley’s William Jagust and UCSF’s Michael Weiner.

William Jagust, UC Berkeley

William J. Jagust, an authority on brain aging and dementia, has been awarded the 2013 Potamkin Prize for Research in Pick’s, Alzheimer’s and Related Diseases by the American Academy of Neurology and the American Brain Foundation.

Jagust, professor of public health and neuroscience at UC Berkeley, will receive the award during the academy’s 65th annual meeting, March 16-23 in San Diego. The annual meeting is the world’s largest gathering of neurologists with more than 10,000 attendees and more than 2,300 scientific presentations on the latest research advances in brain disease.

The Potamkin Prize honors researchers for their work in helping to advance the understanding of Pick’s disease, Alzheimer’s disease and related disorders. The $100,000 prize is an internationally recognized tribute for advancing dementia research.

Jagust is receiving the Potamkin Prize for his research on beta-amyloid, or plaques in the brain, which are a possible cause of Alzheimer’s disease. Jagust uses brain imaging techniques in his studies that help outline amyloid protein and its effects on the brain. He works to find biomarkers that will help detect Alzheimer’s in people with very mild symptoms or no symptoms at all.

“I am extremely honored to be in the company of so many outstanding scientists who have previously received this award, as well as my co-recipients,” said Jagust. “Results from our experiments suggest different ways of thinking about the Alzheimer’s disease process and how to best treat it.”

Two other scientists will also receive a 2013 Potamkin Prize in March: Michael W. Weiner with the San Francisco VA Medical Center in San Francisco and a professor of radiology at UC San Francisco, and Eric M. Reiman with Banner Alzheimer’s Institute in Phoenix.

The Potamkin Prize is made possible by the philanthropic contributions of the Potamkin family of Colorado, Philadelphia and Miami. The goal of the prize is to help attract the best medical minds and most dedicated scientists in the world to the field of dementia research.

View original article