Opportunities for enhancing brain health across the lifespan
Published online by Cambridge University Press: 22 March 2021
As we age, there are characteristic changes in our thinking, reasoning and memory skills (referred to as cognitive ageing). However, variation between people in the timing and degree of change experienced suggests that a range of factors determine individual cognitive ageing trajectories. This narrative review considers some of the lifestyle factors that might promote (or harm) cognitive health. The focus on lifestyle factors is because these are potentially modifiable by individuals or may be the targets of behavioural or societal interventions. To support that, the review briefly considers people’s beliefs and attitudes about cognitive ageing; the nature and timing of cognitive changes across the lifespan; and the genetic contributions to cognitive ability level and change. In introducing potentially modifiable determinants, a framing that draws evidence derived from epidemiological studies of dementia is provided, before an overview of lifestyle and behavioural predictors of cognitive health, including education and occupation, diet and activity.
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.
“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.
From the American Journal of Clinical Nutrition (April 22, 2020):
Our findings imply that higher long-term dietary intakes of flavonoids are associated with lower risks of ADRD and AD in US adults.
Our findings provide new evidence that diets higher in flavonols, anthocyanins, and flavonoid polymers are associated with a lower risk of developing ADRD. These associations were sustained after accounting for a variety of potential confounders including key nutrients related to ADRD risk and overall diet quality. Similar findings were seen with AD risk for flavonols and anthocyanins but the association with flavonoid polymers was no longer statistically significant.
Along with improvements in healthcare and medical technology, the aging of the baby boom generation will result in an unprecedented rise in the number of older Americans (1, 2). Currently, there are >50 million Americans aged ≥65 y, and that is projected to more than double by 2060 (3). A consequence of this increase in older adults is the escalation of age-related diseases (4, 5). Alzheimer disease (AD) and related dementias (ADRD), a group of symptoms in which there is progressive deterioration in cognitive function severe enough to interfere with a person’s daily living activities, are regarded as among the most significant public health challenges largely affecting adults aged >65 y (6). AD is the most common form of dementia, making up ∼60–80% of dementia cases. Currently, 5.8 million Americans are living with AD, and by 2050 that is projected to escalate to 14 million (7).
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.