Filmed on Thursday 3 December 2020, Walk along Paddington Basin, Grand Union Canal, to Little Venice London in the rain. You will see many narrowboats as we walk along the canal.
Route Timestamps 00:00 Paddington Basin 24:15 Delamere Terrace 24:59 Westbourne Terrace Road Bridge 26:14 Blomfield Road 29:25 Warwick Avenue
Stroke is far more common than you might realize, affecting more than 795,000 people in the U.S. every year. It is a leading cause of death and long-term disability. Yet until now, treatment options have been limited, despite the prevalence and severity of stroke.
Not so long ago, doctors didn’t have much more to offer stroke victims than empathy, says Kevin Sheth, MD, Division Chief of Neurocritical Care and Emergency Neurology. “There wasn’t much you could do.” But that is changing. Recent breakthroughs offer new hope to patients and families. Beating the Clock Think of stroke as a plumbing problem in the brain. It occurs when there is a disruption of blood flow, either because of a vessel blockage (ischemic stroke) or rupture (hemorrhagic stroke).
In both cases, the interruption of blood flow starves brain cells of oxygen, causing them to become damaged and die. Delivering medical interventions early after a stroke can mean the difference between a full recovery and significant disability or death. Time matters. Unfortunately, stroke care often bottlenecks in the first stage: diagnosis. Sometimes, it’s a logistical issue; to identify the type, size, and location of a stroke requires MRI imaging, and the machinery itself can be difficult to access.
MRIs use powerful magnets to create detailed images of the body, which means they must be kept in bunker-type rooms, typically located in hospital basements. As a result, there is often a delay in getting MRI scans for stroke patients. Dr. Sheth collaborated with a group of doctors and engineers to develop a portable MRI machine. Though it captures the images doctors need to properly diagnose stroke, it uses a less powerful magnet. It is lightweight and can be easily wheeled to a patient’s bedside.
“It’s a paradigm shift – from taking a sick patient to the MRI to taking an MRI to a sick patient,” says Dr. Sheth. Stopping the Damage Once a stroke has been diagnosed, the work of mitigating the damage can begin. “Brain tissue is very vulnerable during the first hours after stroke,” says vascular neurologist Nils Petersen, MD. He and his team are using advanced neuro-monitoring technology to study how to manage a patient’s blood pressure in the very acute phase after a stroke.
Dr. Petersen’s research shows that optimal stroke treatment depends on personalization of blood pressure parameters. But calculating the ideal blood pressure for the minutes and hours after a patient has a stroke can be complicated. It depends on a variety of factors—it is not a one-size-fits-all scenario. Harnessing the Immune System Launching an inflammatory reaction is how the body responds to injury anywhere in the body – including the brain, following stroke. However, in this case, the resulting inflammation can sometimes cause even more damage.
But what if that immune response could be used to the patient’s advantage? “We’re trying to understand how we can harness the immune system’s knowledge about how to repair tissues after they’ve been injured,” says Lauren Sansing, MD, Academic Chief of the Division of Stroke and Vascular Neurology. Her team is working to understand the biological signals guiding the immune response to stroke.
That knowledge can then direct the development of targeted therapeutics for the treatment of stroke that minimize early injury and enhance recovery. “We want to be able to lead research efforts that change the lives of patients around the world,” says Dr. Sansing.
Learn about these developments and more in the video above.
For more information on aneurysms or #YaleMedicine, visit: https://www.yalemedicine.org/conditio…
Many studies suggest that exercise can help protect our memory as we age. This is because exercise has been shown to prevent the loss of total brain volume (which can lead to lower cognitive function), as well as preventing shrinkage in specific brain regions associated with memory. For example, one magnetic resonance imaging (MRI) scan study revealed that in older adults, six months of exercise training increases brain volume.
Another study showed that shrinkage of the hippocampus (a brain region essential for learning and memory) in older people can be reversed by regular walking. This change was accompanied by improved memory function and an increase of the protein brain-derived neutropic factor (BDNF) in the bloodstream.
The brain is highly dependent on blood flow, receiving approximately 15% of the body’s entire supply – despite being only 2-3% of our body’s total mass. This is because our nervous tissues need a constant supply of oxygen to function and survive. When neurons become more active, blood flow in the region where these neurons are located increases to meet demand. As such, maintaining a healthy brain depends on maintaining a healthy network of blood vessels.
Regular exercise increases the growth of new blood vessels in the brain regions where neurogenesis occurs, providing the increased blood supply that supports the development of these new neurons. Exercise also improves the health and function of existing blood vessels, ensuring that brain tissue consistently receives adequate blood supply to meet its needs and preserve its function.
Recently, a growing body of research has centred on microglia, which are the resident immune cells of the brain. Their main function is to constantly check the brain for potential threats from microbes or dying or damaged cells, and to clear any damage they find.
With age, normal immune function declines and chronic, low-level inflammation occurs in body organs, including the brain, where it increases risk of neurodegenerative disease, such as Alzheimer’s disease. As we age, microglia become less efficient at clearing damage, and less able to prevent disease and inflammation. This means neuroinflammation can progress, impairing brain functions – including memory.
World-renowned philosopher Daniel C. Dennett argues that our inner worlds and religious ideas can all be explained as evolutionary functions of the brain.
“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:
‘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.
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.
READ EXCERPT OF FIRST 30 PAGES
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.
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Boomers Daily 