Neuroscience Professor Seth Tomchik, PhD, focuses on two major research areas, the neuroscience of learning and memory, and diseases that affect learning and memory, including neurofibromatosis type one. Neuroscience is now the largest department on the Florida campus of Scripps Research.
The department’s faculty and staff, together with graduate students enrolled in the institute’s Skaggs Graduate School, push the boundaries of scientific knowledge to benefit humanity. Watch all 11 videos in this series to see their work in more detail. Scripps Research is an independent, nonprofit biomedical research institute ranked the most influential in the world for its impact on innovation. With campuses in La Jolla, California, and Jupiter, Florida, the institute advances human health through profound discoveries that address pressing medical concerns around the globe. Scripps Research also trains the next generation of leading scientists at the Skaggs Graduate School, consistently named among the top 10 U.S. programs for chemistry and biological sciences. Learn more at http://www.scripps.edu.
“We are learning that tactics to avoid dementia begin early and continue throughout life, so it’s never too early or too late to take action,” says commission member and AAIC presenter Lon Schneider, MD, co-director of the USC Alzheimer Disease Research Center‘s clinical core and professor of psychiatry and the behavioral sciences and neurology at the Keck School of Medicine of USC.
LOS ANGELES — Modifying 12 risk factors over a lifetime could delay or prevent 40% of dementia cases, according to an updated report by the Lancet Commission on dementia prevention, intervention and care presented at the Alzheimer’s Association International Conference (AAIC 2020).
Twenty-eight world-leading dementia experts added three new risk factors in the new report — excessive alcohol intake and head injury in mid-life and air pollution in later life. These are in addition to nine factors previously identified by the commission in 2017: less education early in life; mid-life hearing loss, hypertension and obesity; and smoking, depression, social isolation, physical inactivity and diabetes later in life (65 and up).
Schneider and commission members recommend that policymakers and individuals adopt the following interventions:
- Aim to maintain systolic blood pressure of 130 mm Hg or less from the age of 40.
- Encourage use of hearing aids for hearing loss and reduce hearing loss by protecting ears from high noise levels.
- Reduce exposure to air pollution and second-hand tobacco smoke.
- Prevent head injury (particularly by targeting high-risk occupations).
- Limit alcohol intake to no more than 21 units per week (one unit of alcohol equals 10 ml or 8 g pure alcohol).
- Stop smoking and support others to stop smoking.
- Provide all children with primary and secondary education.
- Lead an active life into mid-life and possibly later life.
- Reduce obesity and the linked condition of diabetes.
‘Journal of Neurology, Neurosurgery & Psychiatry” (July 10, 2020):
We tested the hypothesis that apathy, but not depression, is associated with dementia in patients with SVD. We found that higher baseline apathy, as well as increasing apathy over time, were associated with an increased dementia risk. In contrast, neither baseline depression or change in depression was associated with dementia. The relationship between apathy and dementia remained after controlling for other well-established risk factors including age, education and cognition. Finally, adding apathy to models predicting dementia improved model fit. These results suggest that apathy may be a prodromal symptom of dementia in patients with SVD.
Cerebral small vessel disease (SVD) is the leading vascular cause of dementia and plays a major role in cognitive decline and mortality.1 2 SVD affects the small vessels of the brain, leading to damage in the subcortical grey and white matter.1 The resulting clinical presentation includes cognitive and neuropsychiatric symptoms.1
Apathy is a reduction in goal-directed behaviour, which is a common neuropsychiatric symptom in SVD.3 Importantly, apathy is dissociable from depression,3 4 another symptom in SVD for which low mood is a predominant manifestation.5 Although there is some symptomatic overlap between the two,6 research using diffusion imaging reported that apathy, but not depression, was associated with white matter network damage in SVD.3 Many of the white matter pathways underlying apathy overlap with those related to cognitive impairment, and accordingly apathy, rather than depression, has been associated with cognitive deficits in SVD.7 These results suggest that apathy and cognitive impairment are symptomatic of prodromal dementia in SVD.
In this month’s episode, we learn that human brains differentiate musical pitch a way that macaque monkeys do not. In fact, speech and music shaped the human brain’s hearing circuits. Researchers are studying these circuits with an eye on developing treatments for neurological disorders.
Although it might seem to be a story of ever-increasing knowledge of biology, Cobb shows how our ideas about the brain have been shaped by each era’s most significant technologies. Today we might think the brain is like a supercomputer. In the past, it has been compared to a telegraph, a telephone exchange, or some kind of hydraulic system. What will we think the brain is like tomorrow, when new technology arises?
For thousands of years, thinkers and scientists have tried to understand what the brain does. Yet, despite the astonishing discoveries of science, we still have only the vaguest idea of how the brain works. In The Idea of the Brain, scientist and historian Matthew Cobb traces how our conception of the brain has evolved over the centuries.
The result is an essential read for anyone interested in the complex processes that drive science and the forces that have shaped our marvelous brains.
Matthew Cobb is Professor of Zoology at the University of Manchester. His previous books include Life’s Greatest Secret:The Race to Discover the Genetic Code, which was shortlisted for the the Royal Society Winton Book Prize, and the acclaimed histories The Resistance and Eleven Days in August. He is also the award-winning translator of books on the history of molecular biology, on Darwin’s ideas and on the nature of life.
An estimated 80 million people live with a neurodegenerative disease, with this number expected to double by 2050. Despite decades of research and billions in funding, there are no medications that can slow, much less stop, the progress of these diseases. The time to rethink degenerative brain disorders has come. With no biological boundaries between neurodegenerative diseases, illnesses such as Parkinson’s and Alzheimer’s result from a large spectrum of biological abnormalities, hampering effective treatment.
Acclaimed neurologist Dr Alberto Espay and Parkinson’s advocate Benjamin Stecher present compelling evidence that these diseases should be targeted according to genetic and molecular signatures rather than clinical diagnoses. There is no Parkinson’s or Alzheimer’s, simply people with Parkinson’s or Alzheimer’s. An incredibly important story never before told, Brain Fables is a wakeup call to the scientific community and society, explaining why we have no effective disease-modifying treatments, and how we can get back on track.
From a March 5, 2020 American Academy of Neurology release:
“These results are exciting, as they suggest that people may potentially prevent brain shrinking and the effects of aging on the brain simply by becoming more active,” said study author Yian Gu, Ph.D., of Columbia University in New York and a member of the American Academy of Neurology.
“Recent studies have shown that as people age, physical activity may reduce the risk of cognitive decline and dementia. Our study used brain scans to measure the brain volumes of a diverse group of people and found that those who engaged in the top third highest level of physical activity had a brain volume the equivalent of four years younger in brain aging than people who were at the bottom third activity level.”
Older people who regularly walk, garden, swim or dance may have bigger brains than their inactive peers, according to a preliminary study to be presented at the American Academy of Neurology’s 72nd Annual Meeting in Toronto, Canada, April 25 to May 1, 2020. The effect of exercise was equal to four fewer years of brain aging. The study used magnetic resonance imaging (MRI) scans to measure the brains of people with a range of activity levels, including those who were inactive to those who were very active. The scans showed less active people had smaller brain volume.
From the Brain Plasticity Journal (Dec 26, 2019):
In conclusion, increased CRF (cardiorespiratory fitness) following this six-month intervention was associated with enhanced brain glucose metabolism in the PCC (posterior cingulate cortex), a region linked to AD, and cognition among late-middle-aged individuals at risk for AD. If these findings are supported by a larger-scale study, this would provide strong evidence that adults at risk for AD may enhance brain function and cognition by engaging in aerobic exercise training.
PCC glucose metabolism correlated positively with change in VO2peak (the highest value of VO2 attained upon an incremental or other high-intensity exercise test, designed to bring the sub- ject to the limit of tolerance)…Improvement in executive function correlated with increased VO2peak. Favorable CRF adaptation after 26 weeks of aerobic exercise training was associated with improvements in PCC glucose metabolism and executive function, important markers of AD.
Aerobic exercise has been associated with reduced burden of brain and cognitive changes related to Alzheimer’s disease (AD). However, it is unknown whether exercise training in asymptomatic individuals harboring risk for AD improves outcomes associated with AD. We investigated the effect of 26 weeks of supervised aerobic treadmill exercise training on brain glucose metabolism and cognition among 23 late-middle-aged adults from a cohort enriched with familial and genetic risk of AD.