Innovative, paradigm-shifting strategies are required to advance treatment of neurological injury. The neuroregeneration research at Mayo Clinic is at the forefront of healing the nervous system. For an in-depth look at neuroregeneration, see the neuroregenerative medicine at Mayo Clinic booklet.
Mayo Clinic clinicians, scientists, engineers and other specialists in the Center for Regenerative Medicine are taking a multidisciplinary integrative approach to neuroregeneration for a number of devastating neurological conditions. The research is multifaceted, ranging from basic science discovery to clinical applications. Alzheimer's disease. Alzheimer's disease is the major cause of dementia in older adults, with progressive loss of neurons in areas of the brain responsible for learning and memory.
Efforts in Alzheimer's disease research focus on understanding why neurons degenerate in brains with Alzheimer's disease and how to either slow down the process or replace lost neurons. Mayo researchers are investigating the effects of restoring cerebrovascular function, through transplantation of induced pluripotent stem iPS cell-derived vascular progenitor cells, on amyloid pathology and cognitive function in amyloid Alzheimer's disease model mice.
This innovative approach will likely allow for rational designs of vascular regenerative therapy against Alzheimer's disease. Anthony J. Windebank, M. Staff, M. Multiple sclerosis. While scientists understand much about the damage that happens to nerves and their insulating sheath myelin during multiple sclerosis MS and how the immune system causes this damage, the exact reasons for the immune system attack are very poorly understood.
The lack of understanding of the exact cause of MS is a challenge for the development of effective therapies, and Mayo Clinic laboratories are working to better understand this disease. Protecting nerves and myelin from damage, or repairing myelin after it's been damaged, also holds potential for the treatment of MS. Injury to nerves and myelin can be severe in MS and is the major cause of functional impairments. However, spontaneous repair of this damage is sometimes observed in people with MS.
Researchers in the Center for Regenerative Medicine are actively engaged in developing therapies designed to stimulate this repair and thereby promote recovery of lost function. Antibodies that bind to myelin and nerve cells and protect nerves from damage and stimulate myelin regeneration have been identified. A recent study also has found that regeneration of the myelin sheath can be stimulated by small, folded DNA molecules aptamers. Multiple system atrophy. Multiple system atrophy MSA is a progressive, fatal neurodegenerative disorder.
The hallmark of the disease is glial cytoplasmic inclusions. The main component of glial cytoplasmic inclusions is alpha-synuclein.
Aggregation of alpha-synuclein microfibrils leads to a chain of events, including microglial activation, inflammation, and glial and neuronal degeneration. This damage could be a stroke, a severe concussion, or any kind of injury. If we can somehow limit the number of neurons that die early after injury, then we are keeping the damage to a minimum. To help with repair later on after the injury, after the damage is done, some scientists are trying to use stem cells as a treatment for neuronal loss in the brain.
They have the capacity to develop into brand new neurons if scientists treat them with special molecules. This is a little like elementary school students who are not doctors or plumbers yet, but they have the capacity to become any professional in the future, given the right training.
The biggest challenge with replacing dead neurons with stem cells is to have these newcomer neurons integrate, or fit into, the existing brain networks the right way. Looking at the structure of a neuron, you will notice it has a cell body and several arms that it uses to connect and talk with other neurons Figure 1 , left.
The really long arm that sends signals to other neurons is called axon , and axons can be really long. If an axon is damaged along its way to another cell, the damaged part of the axon will die Figure 1 , right , while the neuron itself may survive with a stump for an arm. The problem is neurons in the central nervous system have a hard time regrowing axons from stumps. Why do skin cells not have this problem? Skin cells are much simpler in structure.
First, they need motivation. There are special molecules that help activate growth in neurons. More of these motivating molecules are made when the neurons are active. So, if you keep your brain active, your neurons are more likely to grow. This is true both after injury and in the healthy brain. Some stop signs are part of the sheath, or covering, around neighboring axons, called myelin sheath Figure 1 , left. Some stop signs are part of a scar that gets built like a protective wall around an injury in an effort to keep the damage from spreading.
These scars are made by brain cells called astrocytes star cells, due to their star-like appearance. Scar-building astrocytes are just trying to help, but they also release a chemical into their environment that makes it hard for axons to grow Figure 2. But, there is good news here as well. Scientists are working on strategies to motivate injured neurons to grow by using special growth molecules and to eliminate stop signs for axons in order to make the injury environment more supportive for nerve cell growth [ 1 ].
But work by Fred "Rusty" Gage, PhD, president and a professor at the Salk Institute for Biological Studies and an adjunct professor at UC San Diego, and others found that new brain cells are continually produced in the hippocampus and subventricular zone, replenishing these brain regions throughout life. Instead, when an adult brain cell of the cortex is injured, it reverts at a transcriptional level to an embryonic cortical neuron.
And in this reverted, far less mature state, it can now regrow axons if it is provided an environment to grow into. In my view, this is the most notable feature of the study and is downright shocking.
To provide an "encouraging environment for regrowth," Tuszynski and colleagues investigated how damaged neurons respond after a spinal cord injury. In recent years, researchers have significantly advanced the possibility of using grafted neural stem cells to spur spinal cord injury repairs and restore lost function, essentially by inducing neurons to extend axons through and across an injury site, reconnecting severed nerves.
Last year, for example, a multi-disciplinary team led by Kobi Koffler, PhD, assistant professor of neuroscience, Tuszynski, and Shaochen Chen, PhD, professor of nanoengineering and a faculty member in the Institute of Engineering in Medicine at UC San Diego, described using 3D printed implants to promote nerve cell growth in spinal cord injuries in rats, restoring connections and lost functions.
The latest study produced a second surprise: In promoting neuronal growth and repair, one of the essential genetic pathways involves the gene Huntingtin HTT , which, when mutated, causes Huntington's disease, a devastating disorder characterized by the progressive breakdown of nerve cells in the brain. Tuszynski's team found that the "regenerative transcriptome" -- the collection of messenger RNA molecules used by corticospinal neurons -- is sustained by the HTT gene.
In mice genetically engineered to lack the HTT gene, spinal cord injuries showed significantly less neuronal sprouting and regeneration. Retrieved November 12, from www. A deficiency of this substance can have drastic consequences: The death of dopamine-producing nerve cells in Researchers now ScienceDaily shares links with sites in the TrendMD network and earns revenue from third-party advertisers, where indicated.
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