Although there is no cure, treatments do exist to control symptoms - and they focus on restoring dopamine levels.
But the KCL research team, writing in Lancet Neurology, suggest that changes in the brain's serotonin levels come first - and could act as an early warning sign.
Image copyrightKING'S COLLEGE LONDONImage captionBrain scans show a reduction in serotonin (blue/black area) as Parkinson's progresses
The researchers looked at the brains of 14 people from remote villages in southern Greece and Italy who all have rare mutations in the SNCA gene, making them almost certain to develop the disease.
Half of this group had already been diagnosed with Parkinson's and half had not yet shown any symptoms, making them ideal for studying how the disease develops.
By comparing their brains with another 65 patients with Parkinson's and 25 healthy volunteers, the researchers were able to pinpoint early brain changes in patients in their 20s and 30s.
These were found in the serotonin system, a chemical which has many functions in the brain, including mood, appetite, cognition, wellbeing and movement.
'Could open doors'
Lead study author Prof Marios Politis, from the Institute of Psychiatry, Psychology and Neuroscience at King's, said the abnormalities had been found long before movement problems had begun and before dopamine levels had changed.
"Our results suggest that early detection of changes in the serotonin system could open doors to the development of new therapies to slow, and ultimately prevent, progression of Parkinson's disease," he said.
Prof Derek Hill, professor of medical imaging at University College London, said the research provided some valuable insights but also had some limitations.
"Their results may not scale up to larger studies," he said.
"Secondly, the imaging method they used is highly specialised and limited to a very small number of research centres, so isn't yet usable either to help diagnose patients or even to evaluate novel treatments in large clinical studies.
"The research does, however, provide encouragement for the approach of trying to treat Parkinson's disease at the earliest possible stage, which is likely to be the best chance of preventing the rising number of people whose lives are destroyed by this hideous disease."
Dr Beckie Port, research manager at charity Parkinson's UK, said: "Further research is needed to fully understand the importance of this discovery - but if it is able to unlock a tool to measure and monitor how Parkinson's develops, it could change countless lives."
It’s been said that some things, like love, wisdom and wine, get better with age. But when it comes to memory, there’s a universal belief that decline is inevitable and a normal part of getting older.
However, recent research suggests that memory can improve with the right lifestyle, supplements and other techniques.
Is memory loss a normal part of aging?
The severe loss of memory that occurs in Alzheimer’s disease or vascular dementia is certainly not normal. Neither is the loss that occurs in mild cognitive impairment, which can be a precursor to dementia. It’s a general misperception that forgetting things more often and experiencing greater difficulty learning new things are to be expected as we grow older. These occurrences may be common, but they’re not “normal”.
What causes memory loss?
In addition to Alzheimer’s disease and vascular dementia, other diseases and conditions can cause memory loss,1 including stroke, Parkinson’s disease, HIV, syphilis, multiple sclerosis, head trauma, epilepsy, depression and chronic alcoholism. Less severe conditions, including menopausal hormone decline, mild concussions, insomnia, stress, hypoglycemia (low blood sugar), dehydration, anxiety, multitasking, prescription drug side effects, vitamin B12 deficiency, exposure to toxins, and even high altitudes can impair memory, although this impairment is often reversible when the cause has been addressed.
In Alzheimer’s disease, memory loss is associated with the accumulation in the brain of proteins known as amyloid beta and tau. While amyloid beta is the better known of these proteins, attempts to treat Alzheimer’s disease by reducing the burden of amyloid beta in the brain have met with failure more often than success. Some researchers have turned to tau as a promising target in Alzheimer’s disease. Tau protein forms the neurofibrillary tangles commonly observed in the brains of Alzheimer’s disease patients. Yet, like amyloid beta, it is not yet known whether tau plays a causative role in Alzheimer’s disease.
Vascular dementia is caused by impaired blood flow to the brain. It can be the result of the same process (atherosclerosis) that occurs in the rest of the body of someone who has cardiovascular disease. Strokes and mini-strokes significantly increase the risk of vascular dementia.
Is cognitive decline reversible?
In a recently published interview, Dale E. Bredesen, MD, who is an expert in the mechanisms of neurodegenerative diseases and originator of The Bredesen Protocol™ for improving cognition, stated “Although the dogma has been that there is nothing that prevents, slows, or reverses the course of cognitive decline in diseases such as Alzheimer’s disease, there are clearly multiple studies now—in both anecdotal and controlled trials—that show examples in which there is indeed prevention and/or reversal of decline.”2
What helps memory?
Regular sound sleep and exercise are very important for supporting memory. Other important factors are a healthy diet (which includes eating regularly to avoid episodes of low blood sugar), stress management, taking steps to reduce underlying diseases such as cardiovascular disease and diabetes, staying hydrated and addressing hormone imbalances.
Which nutritional supplements help memory and concentration?
Quite a few supplements have been shown in experimental or clinical research to benefit memory and learning ability or slow their decline. These include choline, dimethylaminoethanol (DMAE), Ginkgo biloba, ashwagandha, Bacopa monnieri, Huperzine A, vinpocetine, phosphatidylserine, omega-3 fatty acids, lithium and others.3-13
How does exercise help memory?
Exercise promotes the formation of neurons in the brain, increases brain volume, boosts cognitive function and helps the brain maintain its ability to adapt to changes.14 It also improves circulation and the delivery of oxygen and supports vascular health.
How can future technology improve memory?
While the loss of memory is a growing concern for an aging population worldwide, research in this area is also growing. Scientists are investigating such aids as brain implants and computer-brain interfaces that expand memory and improve other functions. Online brain training programs are available now that work like exercise in the brain to help improve memory and learning, while tracking progress over time.
Nootropic compounds that may enhance memory have been the subject of research during the past several decades. These so-called “smart-drugs” have the potential to benefit everyone from college students seeking to improve exam scores to elderly men and women suffering from cognitive decline. The future may see the development of more advanced compounds and the use of smart drugs by more people.
Memory is more likely to improve with the adoption of more than just one or two of the therapies discussed in this post. A multifaceted, personalized program such as that developed by Dr Bredesen will improve the odds of maintaining our memories and perhaps even reverse some aspects of memory loss.
References
1. https://www.mayoclinic.org/diseases-conditions/alzheimers-disease/in-depth/memory-loss/art-20046326 2. Gustafson C. Integr Med (Encinitas). 2015 Oct; 14(5): 26–29. 3. Malanga G et al. Drug Metab Lett. 2012 Mar;6(1):54-9. 4. McDaniel MA et al. Nutrition. 2003 Nov-Dec;19(11-12):957-75. 5. Kaschel R. Phytomedicine. 2011 Nov 15;18(14):1202-7. 6. Choudhary D et al. J Diet Suppl. 2017 Nov 2;14(6):599-612. 7. Morgan A et al. J Altern Complement Med. 2010 Jul;16(7):753-9. 8. Xu SS et al. Zhongguo Yao Li Xue Bao. 1995 Sep;16(5):391-5. 9. Subhan Z et al. Eur J Clin Pharmacol. 1985;28(5):567-71. 10.Montgomery SA et al. Int Clin Psychopharmacol. 2003 Mar;18(2):61-71. 11. Zhang YY et al. Genet Mol Res. 2015 Aug 10;14(3):9325-33. 12. Külzow N et al. J Alzheimers Dis. 2016;51(3):713-25. 13. Nunes MA et al. Curr Alzheimer Res. 2013 Jan;10(1):104-7. 14. Marks BL et al. Phys Sportsmed. 2009 Apr;37(1):119-25. https://blog.lifeextension.com/2019/02/can-memory-improve-reversing-cognitive.html
Researchers are discovering fascinating things about the links between sleep, how we remember things
Duncan McCue · CBC News ·
A project at the Royal Ottawa Institute for Mental Health Research aims to uncover exactly how our brains process and synthesize memories. It also aims to shed light on how sleep deprivation may contribute to dementia. (Diane Grant/CBC)
It's time for bed, and in addition to my cosy red pyjamas decorated with hockey sticks, I'm wearing electrodes all over my body.
With wires sprouting from my scalp, chest and legs, I feel more like Frankenstein than Sleeping Beauty.
"Have a good night," sings out Stuart Fogel, as he shuts off the light in my austere bedroom at the Royal Ottawa Institute for Mental Health Research.
Then he's off to the laboratory — where my brain waves will be documented for the next eight hours — to search for clues about how memory works.
"It's hard to communicate the benefit that you can get from sleep, and the importance of sleep, when so many other things seem to be of greater importance in our daily lives," Fogel says.
CBC correspondent Duncan McCue had his brain waves documented as part of a study on sleep and memory. He slept overnight at the Royal Ottawa Institute for Mental Health Research. (Diane Grant/CBC)
Researchers have known for a while that sleep is essential to how we form memories. But Fogel, a professor at the University of Ottawa's Sleep Research Laboratory, is keen to uncover exactly how our brains process and synthesize those memories.
His research comes at a time when about a third of Canadian adults get less than seven hours of sleep a night on average, according to Statistics Canada.
And the consequences of sleep deprivation are far more serious than feeling dozy and worn out.
"What's intriguing is that sleep loss will have an impact on your ability to retain anything that you learn that's new," Fogel says.
The research also aims to shed light on how sleep deprivation may contribute to a condition that's on the rise in Western societies: dementia.
Sleep spindles
Generally, adults spend one-third of their lives sleeping. It's only in the past few decades that scientists have begun to understand some of the reasons why.
"The more we study this, the more we find how there's just so many aspects of sleep that are involved in memory processing," Fogel says.
Fogel has spent several years examining the relationship between memory and "sleep spindles," the brief bursts of brain activity which occur during deep sleep. These one- to two-second electrical pulses happen up to 1,000 times a night, and can be measured on an electroencephalogram (EEG).
Stuart Fogel is studying healthy adults for insights into how sleep affects motor memory skills. He hopes to determine if sleep therapy could help slow the onset of dementia. (Christian Patry/CBC)
Researchers believe these spindles show our brain taking what we learn each day and shifting it from the hippocampus, a limited space where we store recent memories, to the prefrontal cortex. That's the brain's "hard drive," where we store important memories for future reference — whether that's tomorrow, next week, or next year.
Sleep effectively cleans up the hippocampus, leaving us ready to take in fresh data.
"Memory centres that are recruited during learning are reactivated during sleep ... that's actually enhancing that memory trace and strengthening it, so that the next day we're better at the task," Fogel says.
What does that mean for a teenager who's up all night texting, or an adult working into the wee hours?
You may not learn as much.
More specifically, if you sleep six hours or less you'll have fewer spindles — and that means you may not permanently retain as much of what what you experienced that day.
Early warning signs
Fogel's current research focuses on how sleep affects newly formed motor skills, such as learning to play a musical instrument or taking a slapshot.
Which explains why I'm lying in a massive MRI scanner before bedtime, madly tapping my fingers on buttons that move brightly-coloured blocks from one side of a screen to another.
To demonstrate his current research, Fogel has invited me to sleep overnight at the Royal Ottawa, along with two other test subjects — Nick Vanderberg, 23, and Tom Patterson, 60.
Patterson is what Fogel describes as an "optimum aging adult," a person with a good diet and no major health issues. During his working years, though, Patterson says he didn't sleep so well.
Since retiring, he's rediscovered the gym, which has improved his rest. But he also finds himself forgetting stuff.
Tom Patterson, 60, is what scientists describe as an 'optimum aging adult,' a person with a good diet and no major health issues. However, he worries about his memory. (Christian Patry/CBC)
"I talk about it a lot [with people my age]. Going into a room and saying, 'Hey, why did I come into this room again? What am I looking for?' That happens. It really does happen," Patterson says.
Fogel is studying healthy adults for insights into how sleep affects their motor memory skills. He hopes to determine if sleep therapy could help slow the onset of dementia.
"What we're hoping is that's going to give us a good sense of some important bio-markers for the early warning signs … that could be possible ways of staving off dementia, or mitigating the consequences, or perhaps finding novel treatments," Fogel says.
He enlisted Vanderberg, a doctoral student, to show how differently a young brain deals with memory and sleep.
Nick Vanderberg, a 23-year-old doctoral student, was part of the test to show how differently a young brain deals with memory and sleep. (Diane Grant/CBC)
In addition to the MRI scan, which allows his team to take pictures of brain activity, Fogel explains that the three of us will take a motor-skills test that involves repeatedly finger-tapping a specific sequence of numbers into a small keypad.
He asks us to enter the numbers – 4 1 3 2 4 – over and over, as quickly as we can. The computer measures our speed and accuracy as we tap furiously for 10 minutes.
"When you really accelerate your performance is when you actually start to chunk the numbers to make the execution of the sequence more efficient," Fogel tells us.
I feel as if I'm getting faster until, by the end, my fingers are numb.
Once all three of us brush our teeth and head to separate bedrooms, research assistants glue electrodes to specific spots on our bodies.
The novel part of Fogel's research is the combined use of the Royal's state-of-the-art MRI and the EEG. The electrodes, along with other equipment, measure our brain traces, eye movements, muscle activity, heart rate, leg movements and breathing.
After making sure the electrodes are on tight, it's time for us to nod off – and for Fogel to discover whether his lab rats learned anything.
WATCH | A neurologist explains the impact of a good sleep on the body:
The sleep boost
Fogel bursts into my room at 6:30 a.m.
"Good morning! Ready for your test?"
I rub my eyes. I slept about eight hours, waking once to use the washroom. I recall it took a while to doze off again.
I groggily sit down at the computer. I hear Patterson and Vanderberg do the same in their bedrooms.
I clutch the keypad, tapping the sequence from the night before – 4 1 3 2 4. I feel faster, but I'm relieved when the student assistant tells me to stop so she can calculate our results.
These scans show brain areas that are activated when learning a new task. The warmer the colour, the stronger the activation. Ottawa researchers are exploring how reduced activation in older adults might explain age-related cognitive deficits. (Royal Ottawa Institute for Mental Health Research)
As we wait, Fogel shows me what the EEG measured during my sleep.
"Your brain was probably pretty tired, I would say," he laughs.
He traces his finger along the squiggly lines that represent my brain waves. Within minutes of hitting the pillow, I was in Stage Two, a light sleep where spindles start to occur.
"You've got really nice, big spindles here ... these big bursts of activity," Fogel says, which sounds encouraging.
"That indicates you're probably reprocessing that information, reactivating those memory traces, integrating them into long-term memory stores."
We convene in the lab to hear the results. Patterson, the senior of the group, had a "broken and interrupted sleep." Vanderberg, the youngster, slept like a rock.
The graph shows all three of us improved our finger speed when our brains began to first process the new task, but our sleep gains were a different story.
The 23-year-old's fingers were even faster in the morning. Mine, too. But, as expected, the 60-year-old was tapping at the same rate as the night before.
Fogel goes over the test results with McCue, Patterson and Vanderberg. Patterson performed slower on the test and did not get a boost from sleep, showing how brain function naturally changes as people age. (Diane Grant/CBC)
As we age, Fogel explains, we don't get the same brain boost from sleep as when we were younger. That's because sleep spindles decrease in both magnitude and frequency.
"That's what we think is the important ingredient … the age-related changes in sleep are actually not allowing that reactivation and strengthening of the memory traces to take place in the same way as when you're younger," Fogel says.
While much remains to be learned about how sleep could be related to Alzheimer's and other forms of dementia, Fogel says it's important to emphasize what scientists do know: sleep is critical for everyone to improve their intellectual and physical performance.
Right now, that's a problem – Canadian adults are getting about an hour less sleep on average than in 2005, according to Statistics Canada.
"Our lives are being filled with more and more information, more and more activities," Fogel says.
"We really need less and less of that, in order to not compete with our time to get the sleep that we need."
PUBLISHED: 14:55 GMT, 24 December 2018 | UPDATED: 15:15 GMT, 24 December 2018
They're not most people's favourite part of Christmas dinner but Brussels sprouts have provided the inspiration for an anti-Alzheimer's drug.
Scientists have developed a medication with 'very good potential' for stopping the breakdown of nerves and brain cells that may lead to the disease.
The drug is made up of 'supercharged' vitamin A, which is found in vegetables like sprouts and carrots.
When broken down by the body, vitamin A turns into a chemical called retinoic acid, which is crucial for the development of the nervous system.
After a two-year £250,000 project to develop vitamin A synthetically, experts hope they are one step closer to treating Alzheimer's, Parkinson's and motor neurone disease.
+1
Brussels sprouts are a rich source of vitamin A which, when broken down by the body, turns into retinoic acid. This is vital for maintaining and regenerating nerves and brain cells. Scientists are therefore making a synthetic version of the nutrient to treat Alzheimer's disease
Researchers at Aberdeen and Durham universities have reported their progress in the ongoing research project.
'We are moving forward with a new therapeutic which could be used to help people with Alzheimer's disease,' said lead author Professor Peter McCaffery, who researches vitamin A at Aberdeen university, said.
'Our work is still at an early stage but we believe this is a positive development and the new drugs seem to protect [nerve cells].'
Retinoic acid is involved in the development of people's eyes and brains in the womb. It also continues to be important for the growth and regeneration of nerves, which control senses, movement and brain activity.
Conditions like Alzheimer's, Parkinson's and motor neurone disease can be triggered by the breakdown of these nerves, which may cause people to lose control of their muscles, disrupt and reduce brain activity, and even be fatal.
Higher levels of retinoic acid in the body could halt nerve damage and boost the number of nerve cells, the researchers hope.
'It's obviously very important to find ways of tackling neurological conditions,' Professor McCaffery added. 'And these super versions of vitamin A are making a difference, at least in the laboratory.
'We have basically been trying to create a massively amplified version of what vitamin A already does for the body.
'We now want to test them further and apply for the necessary patents, but I am pleased with how things have progressed since 2016.'
The drug may also benefit ALS - or Lou Gehrig's disease - which affects the muscles of the arms, legs, mouth and respiratory system.
The research was carried out alongside the chemical development company High Force Research. The results of their lab research will be published next year.
WHAT IS ALZHEIMER'S?
Alzheimer's disease is a progressive, degenerative disease of the brain, in which build-up of abnormal proteins causes nerve cells to die.
This disrupts the transmitters that carry messages, and causes the brain to shrink.
More than 5 million people suffer from the disease in the US, where it is the 6th leading cause of death.
WHAT HAPPENS?
As brain cells die, the functions they provide are lost.
That includes memory, orientation and the ability to think and reason.
The progress of the disease is slow and gradual.
On average, patients live five to seven years after diagnosis, but some may live for ten to 15 years.
EARLY SYMPTOMS:
Loss of short-term memory
Disorientation
Behavioral changes
Mood swings
Difficulties dealing with money or making a phone call
LATER SYMPTOMS:
Severe memory loss, forgetting close family members, familiar objects or places
Becoming anxious and frustrated over inability to make sense of the world, leading to aggressive behavior
Adrenaline, which paramedics inject when CPR (Cardiopulmonary resuscitation) and electric shocks are failing to work, barely improves the chances of living but nearly doubles serious neurological harm among those who do survive.
Scientists believe it may damage the function of blood vessels in the brain, leaving patients in a vegetative state.
Either that or adrenaline causes damage because the heart can survive without oxygen for longer than the brain, meaning that although it can be restarted the brain is likely to be permanently impaired.
The drug is given to around eight in ten of the 30,000 people who suffer a cardiac arrest - when the heart stops beating - outside hospital every year in the UK, of whom only 10 per cent survive.
The findings of the study by the University of Warwick means health leaders may ban ambulance crews from using it.
The authors said the results further highlighted the importance of CPR and defibrillation skills among the public.
Published in the New England Journal of Medicine, the study involved 8,000 patients across five ambulance areas in England between 2014 and 2017.
Paramedics attending a cardiac arrest victim administered either an adrenaline shot or a placebo injection.
Of the 128 patients who were given adrenaline and survived, 40 - 30.1 per cent - had severe brain damage, compared with 17 of the 91 survivors - 18.7 per cent - who were given a placebo.
Professor Gavin Perkins, an expert in critical care medicine at Warwick, said: “What we’ve shown is that adrenaline can restart the heart but it’s no good for the brain.”
Previous research indicates that for every minute a cardiac arrest victim goes without treatment, their chances of survival drop by 10 per cent.
Paramedics will typically make three attempts to restart the heart using a defibrillator before injecting adrenaline, a process that takes around six to eight minutes.
Professor Jerry Nolan, from the Royal United Hospital Bath, who co-authored the paper, said it “highlights the critical importance of the community respond to cardiac arrest”.
“Unlike adrenaline, members of the public can make a much bigger difference to survival through learning how to recognise cardiac arrest, perform CPR and deliver an electric shock with a defibrillator,” he said.
KING'S COLLEGE LONDON
