High blood pressure in mid-30s may pose risk to brain health

HEALTH

PEOPLE in their mid-30s need to watch their blood pressure to protect brain health in later life, says a study.
It found the “window of opportunity” to safeguard brain health runs from then until the early-50s.
Following 500 people born in 1946, it linked higher blood pressure in early mid-life to later blood vessel damage and brain shrinkage.
Experts said high blood pressure in the “critical period” of the 30s and 40s could “accelerate damage” to the brain.
This is not the first time raised blood pressure in middle age has been linked to increased dementia risk, but the scientists wanted to understand more about when and how it might happen.
Throughout this study, published in Lancet Neurology, participants had their blood pressure measured and underwent brain scans.
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Increases in blood pressure between the ages of 36 and 43 were associated with brain shrinkage.
‘Accelerating damage’
Everyone’s brain shrinks a little as they age, but it is more pronounced in those with neurodegenerative diseases like vascular dementia.
And while those studied did not show signs of cognitive impairment, the researchers say brain shrinkage usually precedes that – so they will be monitoring the people in the study over the coming years to watch for signs.
People in their mid-30s need to watch their blood pressure to protect brain health in later life, says a study.
It found the “window of opportunity” to safeguard brain health runs from then until the early-50s.
Following 500 people born in 1946, it linked higher blood pressure in early mid-life to later blood vessel damage and brain shrinkage.
Experts said high blood pressure in the “critical period” of the 30s and 40s could “accelerate damage” to the brain.
This is not the first time raised blood pressure in middle age has been linked to increased dementia risk, but the scientists wanted to understand more about when and how it might happen.
Throughout this study, published in Lancet Neurology, participants had their blood pressure measured and underwent brain scans.

RAISED blood pressure between 43 and 53 was also linked to more signs of blood vessel damage or “mini strokes” when in people reaching their 70s.
Prof Jonathan Schott, a clinical neurologist at the UCL Queen Square Institute of Neurology, led the research.
He said: “Blood pressure, even in our 30s, could have a knock-on effect on brain health four decades later. Monitoring and interventions aimed at maximising brain health later in life need to be targeted at least by early mid-life.”
Prof Schott told the BBC: “NHS health checks are currently offered from the age of 40, and the uptake is, at most, 50%. Our data suggests blood pressure should be measured much earlier.”
Paul Leeson, professor of cardiovascular medicine at the University of Oxford, said: “We have known for some time that people who have higher blood pressure tend to have different brain structure in later life.
“What doctors have been debating is whether treating high blood pressure in young people actually prevents these brain changes.
“The alternative, which is what we tend to do right now, is wait until later in life to start to take high blood pressure seriously because we know that by then, the more severe brain changes are definitely developing.
“These findings do support the idea that there may be critical periods in life, such as in your 30s and 40s, when periods of high blood pressure are accelerating damage within the brain.”
Dr Carol Routledge, director of research at Alzheimer’s Research UK, said: “High blood pressure in midlife is one of the strongest lifestyle risk factors for dementia, and one that is in our control to easily monitor and manage.
“Research is already suggesting that more aggressive treatment of high blood pressure in recent years could be improving the brain health of today’s older generations.
“We must continue to build on this insight by detecting and managing high blood pressure even for those in early midlife.” –BBC

Scratching the surface of how your brain senses an itch

LIGHT touch plays a critical role in everyday tasks, such as picking up a glass or playing a musical instrument, as well as for detecting the touch of, say, biting insects. Researchers have discovered how neurons in the spinal cord help transmit such itch signals to the brain. The findings could help contribute to a better understanding of itch and could lead to new drugs to treat chronic itch, which occurs in such conditions as eczema, diabetes and even some cancers.
Light touch plays a critical role in everyday tasks, such as picking up a glass or playing a musical instrument. The sensation is also an essential part of the body’s protective defense system, alerting us to objects in our environment that could cause us to fall or injure ourselves. In addition, it is part of the detection system that has evolved to protect us from biting insects, such as those that cause malaria and Lyme disease, by eliciting a feeling of an itch when an insect lands on your skin.
Salk researchers have discovered how neurons in the spinal cord help transmit such itch signals to the brain. Published in the journal Cell Reports on July 16, 2019, their findings help contribute to a better understanding of itch and could lead to new drugs to treat chronic itch, which occurs in such conditions as eczema, diabetes and even some cancers.
“The takeaway is that this mechanical itch sensation is distinct from other forms of touch and it has this specialized pathway within the spinal cord,” says Salk Professor Martyn Goulding, holder of the Frederick W. and Joanna J. Mitchell Chair and a senior author of the new work.
Goulding and his colleagues had previously discovered a set of inhibitory neurons in the spinal cord that act like cellular brakes, keeping the mechanical itch pathway in the spinal cord turned off most of the time. Without these neurons, which produce the neurotransmitter neuropeptide Y (NPY), the mechanical itch pathway is constantly on, causing chronic itch. What the researchers didn’t know was how the itch signal, which under normal circumstances is suppressed by the NPY neurons, is transmitted to the brain to register the itch sensation.
David Acton, a postdoctoral fellow in the Goulding lab, hypothesized that when the NPY inhibitory neurons are missing, neurons in the spinal cord that normally transmit light touch begin to act like an accelerator stuck in the “on” position. Acton then identified a candidate for these “light touch neurons,” a population of excitatory neurons in the spinal cord that express the receptor for NPY, the so-called Y1 spinal neurons.
To test whether these neurons were indeed acting like an accelerator, Acton undertook an experiment that involved selectively getting rid of both the NPY “brake” and Y1 “accelerator” neurons. Without Y1 neurons, mice didn’t scratch, even in response to light-touch stimuli that normally make them scratch. Moreover, when Acton gave the animals drugs that activated the Y1 neurons, the mice scratched spontaneously even in the absence of any touch stimuli. The Goulding team was then able to show that the NPY neurotransmitter controls the level of Y1 neuron excitability; in other words, NPY signaling acts as a kind of thermostat to control our sensitivity to light touch. Data from other labs has found that some people with psoriasis have lower than average levels of NPY. This may mean their brakes on mechanical itching are less effective than other people’s, a potential cause of their itching.
While Y1 neurons transmit the itch signal in the spinal cord, other neurons are thought to be responsible for mediating the final response in the brain but more research is needed to continue mapping out the full pathway, according to the researchers. Understanding this will help suggest targets for drugs to turn down the sensation of itch in people who are overly responsive and could lead to ways to address chronic itch.
“By working out mechanisms by which mechanical itch is signaled under normal circumstances, we might then be able to address what happens in chronic itch,” says Acton.
– Science Daily