Can Slow Walking Speed in Elderly Signal Alzheimer’s Disease Hallmarks?

Newswise, December 8, 2015 – How fast elderly people walk may be related to the amount of amyloid they have built up in their brains, even if they don’t yet have symptoms of Alzheimer’s disease, according to a study published in the December 2, 2015, online issue of Neurology®, the medical journal of the American Academy of Neurology.

 

The study involved 128 people with an average age of 76 who did not have dementia but were considered at high risk for developing it because they had some concerns about their memory. 

The participants had positron emission tomography (PET) scans of their brains to measure amyloid plaques in the brain. These plaques consist of dense deposits of a protein called beta amyloid, and their progressive buildup in the brain has been associated with the development of Alzheimer’s disease. 

Of the participants, 48 percent had a level of amyloid often associated with dementia.

Participants were also tested on thinking and memory skills and how well they could complete everyday activities. A total of 46 percent of the participants had mild cognitive impairment, which can be a precursor to the dementia that occurs in Alzheimer’s disease.

Walking speed was measured with a standard test that times people on how fast they can walk about 13 feet at their usual pace. The average walking speed was 3.48 feet per second. All but two of the participants tested in the normal range of walking speed.

The researchers found an association between slow walking speed and amyloid in several areas of the brain, including the putamen, a key region involved in motor function. 

The researchers compared how fast people walked both with and without taking into account the amount of amyloid and found that the amyloid level accounted for up to 9 percent of the difference in walking speed.

The relationship between amyloid levels and walking speed did not change when researchers took into account age, education level, or amount of memory problems.

“It’s possible that having subtle walking disturbances in addition to memory concerns may signal Alzheimer’s disease, even before people show any clinical symptoms,” said study author Natalia del Campo, PhD, of the Gerontopole and the Centre of Excellence in Neurodegeneration of Toulouse (University Hospital Toulouse) in France.

Del Campo noted that the study looked only at a snapshot in time and does not prove that amyloid plaques cause the slowdown in walking speed; it shows the association. She also noted there are many other causes of slow walking in older adults.

The study was based on a larger trial called the Multidomain Alzheimer Preventive Trial, which was supported by the French Ministry of Health and Pierre Fabre Research Institute. 

The imaging was supported by Avid Radiopharmaceuticals/Eli Lilly and Company. Biological sample collection was supported by Exhonit Therapeutics. The promotion of the study was supported by the University Hospital in Toulouse.

To learn more about Alzheimer’s disease, please visit www.aan.com/patients.

The American Academy of Neurology, an association of more than 28,000 neurologists and neuroscience professionals, is dedicated to promoting the highest quality patient-centered neurologic care. 

A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as Alzheimer’s disease, stroke, migraine, multiple sclerosis, brain injury, Parkinson’s disease and epilepsy.

Parkinson’s Disease Brain Cells at Risk of Burnout, Like an Overheating Motor

 Researchers find that the brain cells most at risk in the disease consume unusually high amounts of energy, gradually exhausting and killing themselves.

Newswise, August 28, 2015 — The death of brain cells in Parkinson’s disease may be caused by a form of cellular energy crisis in neurons that require unusually high quantities of energy to carry out their job of regulating movement, researchers at the University of Montreal reported today. 

The neurodegenerative disorder affects over 100,000 Canadians and over 1,000,000 Americans. 

“Like a motor constantly running at high speed, these neurons need to produce an incredible amount of energy to function. They appear to exhaust themselves and die prematurely,” said lead researcher Louis-Éric Trudeau, a professor at the university’s Departments of Phamacology and Neurosciences. 

The research article, published today in Current Biology, includes contributions from Consiglia Pacelli, Nicolas Giguère and Marie-Josée Bourque, also of the University of Montreal, and Martin Lévesque and Ruth Slack, of Laval and Ottawa universities, respectively.

The findings are in some ways a culmination of Trudeau’s 17 years of studying the part of the brain that causes Parkinson’s disease, schizophrenia and drug addiction. His findings could open the door to the creation of better animal models of Parkinson’s disease and the identification of new treatment strategies. 

“For some unknown reason, it has been incredibly difficult to reproduce the symptoms of Parkinson’s in mice, even when introducing in the genome of these animals the same mutations found in humans afflicted by familial forms of the disease. Our discovery provides a new lead to potentially overcome such difficulties” Trudeau explained.

Improved animal models open a variety of new avenues of research. “It’s possible that new medications could be developed to help the neurons in question reduce their energy consumption or produce energy more efficiently, which would reduce accumulated damage over the years,” Trudeau said. 

His team is already looking at the possible next steps with Professor Slack and her colleague Professor David Park.

Targeting the dark side
Unlike Alzheimer’s, which has a wider-ranging impact on billions of brain neurons, the primary symptoms or Parkinson’s are caused by the death of tens or hundreds of thousands of neurons in a few more restricted areas of the brain, including regions called the substantia nigra (literally “the black substance”), the locus ceruleus and the dorsal nucleus of the vagus nerve.

Key to the mystery may be mitochondria, the powerhouses that allow cells to grow and neurons to conduct electrical signals and release their chemical messengers such as dopamine, noradrenaline and acetylcholine. For the past three years, the research team carried out numerous experiments in order to identify why mitochondria in neurons of the substantia nigra work so hard and apparently lead neurons to “overheat”.

They discovered that this overheating could be caused by the fact that these neurons have an amazingly complex structure with a large number of extensions and neurotransmitter release sites, much like a tree with numerous branches. 

Providing energy to these numerous branches may make the neurons particularly vulnerable, leading, in the context of aging, to malfunction and cell death, thus triggering Parkinson’s, with the onset of symptoms generally at around age sixty. 

“Our work supports the theory that very complex neurons like those found in the substantia nigra force the mitochondria to constantly work at burnout rates to produce energy. This would explain the accelerated cell deterioration,” Trudeau explained. 

“To use the analogy of a motor, a car that overheats will burn significantly more fuel, and, not surprisingly, end up at the garage more often.”

Professor Trudeau notes that the most common neurodegenerative diseases are particularly challenging for researchers, because in a way, their increasing prevalence is the result of increased life expectancy. 

“From an evolutionary standpoint, some of our neurons are perhaps just not programmed to last 80, 90 or 100 years, as we are seeing more and more. It’s to be expected that certain parts of our body are less able to withstand the effects of time,” he said. 

However, given the more localized nature of Parkinson’s disease (compared to other afflictions), an effective treatment may be discovered in the not-too-distant future. 

Nevertheless, Trudeau points out that his primary goal is to develop a fundamental understanding of the mechanisms of the brain in order to shed new light on neurological disorders.

About this study:
Professor Louis-Éric Trudeau and his team are affiliated with the University of Montreal’s Groupe de Recherche sur le Système Nerveux Central, Department of Pharmacology and Department of Neurosciences. Trudeau and his colleagues published “"Elevated mitochondrial bioenergetics and axonal arborization size are key contributors to the vulnerability of dopamine neurons" inCurrent Biology on August 27, 2015.

The research team received support for this project from Brain Canada in partnership with the Krembil Foundation, as well as from Parkinson Society Canada.

The University of Montreal is officially known as Université de Montréal.