The concept of chronic traumatic encephalopathy (CTE) was first described in the early 1900s as an aftermath of boxing termed dementia pugilistica. However, it was not until much later, in 2005, that pathologist Bennet Omalu discovered the first evidence in Pittsburgh Steelers’ player Mike Webster. Since that time, CTE has become fairly well-known as more people, commonly athletes and military veterans, are accurately diagnosed.
PRA’s Medical Director of Medical Affairs Therapeutic Expertise, Ly Ngo, discusses the similarities and differences between Chronic Traumatic Encephalopathy and Alzheimer’s Disease; and explores how their symptoms can be approached using a similar treatment plan.
Symptoms of CTE are progressive, occur in stages, and typically fall into one of the following categories: mood, behavior, cognition, and motor. Early stages include headache, loss of attention and concentration, depression, mood swings, explosivity, and memory loss. Later stage symptoms may include visuospatial abnormality, dementia, executive dysfunction, paranoia, aggression, speech, and gait abnormality.
Because CTE typically presents with memory impairment (85%) and executive dysfunction as well as difficulty with attention and concentration, it may be initially mistaken for Alzheimer’s dementia (AD). AD is a common neurodegenerative disorder marked by a progressive decline in cognitive function. However, even though some of the symptoms may overlap, CTE is commonly regarded as having a different “flavor” from AD.
The diagnosis of CTE is based on various aspects, including a history of multiple impacts to the head, the presence of clinical features for at least 12 months, and having no other neurologic disorder to account for the clinical features. Potential biomarkers include:
- Normal beta-amyloid CSF levels (unless concomitant AD diagnosis).
- Elevated CSF p-tau/tau ratio.
- Negative amyloid imaging.
- Cortical atrophy beyond expected for age as seen on imaging (frontal, thalamic, hippocampal, or amygdala).
Additionally, experimental biomarkers include positive tau imaging by PET scan and cortical thinning based on MRI measurements. Confirmation of the diagnosis is by autopsy and neuropathology.
Pathologically, CTE and AD both exhibit tau protein. However, CTE displays a pathognomonic perivascular distribution of astrocytic and neurofibrillary tangles at the depths of the cortical sulci starting in the frontal cortex and later involving the temporal lobes. A cavum septum pellucidum may also be seen. In comparison, AD characteristically involves the temporal lobes, notably the entorhinal cortex.
Currently, the treatment for both CTE and AD is supportive. Many of the same medications are used to treat the symptoms of both diseases, however for CTE, these are commonly off-label indications. Cholinesterase inhibitors are used for memory impairment, while memantine may be used for moderate to severe dementia in both cases. SSRIs are used to treat depression, anxiety, and atypical neuroleptics may be given for explosivity and violence. The only known prevention for CTE is to avoid head injury.
CTE and AD are clearly two distinct disease entities; however, a history of neurotrauma has been linked to the development of dementia and accelerated Aβ deposition, causing researchers to further examine the link between CTE and AD as well as other neurodegenerative disorders, including Lewy body dementia and ALS. Although these are two distinct diseases, one similarity stands out – that there is still much research that is needed in the understanding, diagnosis, and treatment of these diseases.
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