CTE A Neurodegenerative Disease
As we suggest, the differences between neurodegenerative diseases are few. It appears that genetics, neurotoxins and head trauma can trigger brain disease, including Alzheimer’s disease, Parkinson’s disease and Creutzfeldt-Jakob disease (CJD). The real difference is which region of the brain comes under attack first and the speed of the attack. No two cases are identical.
CTE is part of the global surge in neurodegenerative disease. The biggest question is whether CTE is infectious like the other forms of neurodegenerative disease. There is no reason to assume that it is not an infectious disease. Caregivers beware.
With CTE, head trauma is blamed as the causative agent, but the disease progression is very similar to the other neurodegenerative diseases. However, with CTE, the neurodegeneration starts in the outermost region of the brain. Alzheimer’s disease begins in the hippocampus, which controls memory. Parkinson’s disease initially affects nerve cells deep within the brain called the basal ganglia and the substantia nigra — the region of the brain that controls movement.
Once neurodegeneration begins, the pathology is similar across the prion spectrum. The different symptoms are due to the different regions of the brain that are hit first by degeneration. Other differences are explained by the patient’s metabolism and lifestyle, including dietary choices.
Both Alzheimer’s disease and chronic traumatic encephalopathy (CTE) are classified as “tauopathies,” a category of diseases characterized by the improper folding and clumping together of a protein called tau (rhymes with how) inside the nerve cells of the brain. The resulting tau aggregates, known as neurofibrillary tangles, are toxic to neurons and are thought to be responsible for the behavioral changes and cognitive decline seen in both disorders. These toxic proteins are likely infectious, which makes CTE another form of transmissible spongiform encephalopathy (TSE). The operative word is “transmissible.” There is no proof to the contrary.
Thus far, pathologists have been able to confirm the diagnosis only posthumously, by identifying the tau signature in donated brains.
Using positron emission tomography (PET scans), researchers found “elevated amounts of abnormal tau protein” in the parts of the brain associated with the disease, known as CTE, compared to men of similar age who had not played football. The authors of the study and outside experts stressed that such tau imaging is far from a diagnostic test for CTE.
Once CTE manifests itself, the disease pathology is almost identical to Creutzfeldt-Jakob disease and Alzheimer’s disease. The primary difference is the region of the brain under attack.
The senior author of the new study, Stanley Prusiner, MD, director of the Institute for Neurodegenerative Diseases (IND), part of the UCSF Weill Institute for Neurosciences, has long held that misfolded tau spreads through the brain because it forms prions, self-propagating proteins that cause TSE. Prusiner earned the Nobel Prize in 1997 for discovering the role of prions in neurodegeneration.
The new research, the first to document tau prions in CTE patients, made use of an experimental platform designed to test prion transmission in human cell cultures. As reported on November 28, 2016 in the online Early Edition of Proceedings of the National Academy of Sciences, misfolded tau from the brains of either AD or CTE patients propagated in these cell cultures and formed aggregates under identical conditions.
More than 40 percent of retired NFL players tested with advanced scanning technology showed signs of traumatic brain injury, a much higher rate than in the general population, according to a new study.
Scientists have found that protein clumps associated with Alzheimer’s disease also are found in the brains of people who have had a head injury and are at risk of developing chronic traumatic encephalopathy (CTE). Although previous research has shown that these clumps, called amyloid plaques, are present shortly after a brain injury. This study shows the plaques are still present more than a decade after the injury.
The findings, by researchers from Imperial College London, may help explain why people who have suffered a serious brain injury appear to be at increased risk of dementia. Although extensive research now suggests major head injury increases dementia risk in later life, scientists do not know the biological changes that cause this effect.
“The consequences of a head injury have been called a hidden disability – although patients may seem to have outwardly made a good recovery, when we see them in clinic years later they can have persistent problems which affect their daily life, for example impairments in concentration and memory,” said Dr Gregory Scott, the lead author of the paper, from the Department of Medicine at Imperial.
“Research is increasingly showing that a blow to the head, such as that sustained in a road accident, triggers biological processes in the brain that burn away in the background for years,” added Dr Scott.
“Although previous research has shown that some head injury patients have these amyloid plaques shortly after the incident, these findings suggest these plaques are still present in the brains of patients over 10 years later. This helps shed light on why brain injury patients seem to be at increased risk of dementia – and may help us develop treatments that reduce this risk.”
In the research, published in the journal Neurology, the team studied nine patients with moderate to severe traumatic brain injuries. Many had sustained these in road traffic accidents, such as being hit by a car, between 11 months to 17 years prior to the study. Although they had no physical disabilities from the injury, many still suffered daily problems with memory and concentration.
The patients, who were aged between 38-55, underwent a brain scan that used a technique that allows scientists to view amyloid plaques. These proteins are thought to be a hallmark of Alzheimer’s disease, and their formation may trigger other changes that lead to the death of brain cells.
The team also scanned the brains of healthy volunteers, and people with Alzheimer’s disease. The patients with head injury were found to have more amyloid plaques than the healthy volunteers, but fewer than those with Alzheimer’s disease.
In the head injury patients, the amyloid plaques were found to be centered mainly in two brain areas: the posterior cingulate cortex – a highly active area in the centre of the brain involved in controlling attention and memory, and the cerebellum – a region at the base of the brain involved in motor control and coordination.
In a second part of the study, the team assessed damage to so-called white matter. This is the ‘wiring’ of the brain, and enables brain cells to communicate with each other. The results showed that amyloid plaque levels in the posterior cingulate cortex were related to the amount of white matter damage, suggesting that injury to the brain’s wiring may be linked to the formation of amyloid plaques.
Although this is small-scale study, explained Dr Scott, it provides hope for developing treatments in the future that may help treat the long-term effects of head injuries.
“This is a preliminary study, and it’s important to stress that these head injury patients didn’t have Alzheimer’s disease. However it supports the idea that the window of treatment for brain injury is potentially months or even years after the initial event. If we can find out exactly what processes are going on in the brain, it may be that we can intervene and improve long-term outcomes for patients.
“The works also highlights how damaging brain injury can be – and fuels the public health debate about what we can do to protect ourselves against head injuries.”
According to a new study published in the Canadian Medical Association Journal, adults who experience a concussion have a long-term suicide risk that is three times higher than that of the general population. That risk increases by a further third if the concussion occurs on a weekend.
CTE is a progressive degenerative disease of the brain found in athletes (and others) with a history of repetitive brain trauma, including symptomatic concussions as well as asymptomatic subconcussive hits to the head. CTE has been known to affect boxers since the 1920s. However, recent reports have been published of confirmed CTE in retired professional football players and other athletes who have a history of repetitive brain trauma.
This trauma triggers progressive degeneration of the brain tissue, including the build-up of an abnormal protein called tau. These changes in the brain can begin months, years, or even decades after the last brain trauma or end of active athletic involvement. The brain degeneration is associated with memory loss, confusion, impaired judgment, impulse control problems, aggression, depression, and, eventually, progressive dementia.
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Gary Chandler is a prion expert. He is the CEO of Crossbow Communications, author of several books and producer of documentaries about health and environmental issues around the world. Chandler is connecting the dots to the global surge in neurodegenerative disease, including Alzheimer’s disease, Parkinson’s disease, Creutzfeldt-Jakob disease, chronic wasting disease and other forms of prion disease. The scientific name for prion disease is transmissible spongiform encephalopathy. The operative word is “transmissible.” Even the global surge in autism appears to be related.