Evidence keeps piling up showing that Traumatic Brain Injuries (TBIs) from house falls, car and bicycle accidents, military exercises and sports like American football are increasingly leading to dementia, Alzheimer’s Diseases and other cognitive disorders. In this piece, i will first look at the scientific litterature that shows the existence of a causal relationship between TBIs and dementia. (Section A). Thereafter, i will examine pathophysiology and mechanisms (Section B) and wrap up with a word on how holistic medicine can help to promote neurogenesis and some semblance of brain recovery for the patients who have been diagnosed with TBI’s and Alzheimer’s Disease. (Section C)
Traumatic Brain Injuries and Alzheimer’s Disease
Researchers from the University of Helsinki and the Helsinki University Hospital recently published a study that substantiates the relationship between TBIs and degenerative brain diseases. Encompassing the entire Finnish population, this study combined several nationwide registers to monitor more than 40,000 working-age adults, who survived the initial TBI, for ten years. Importantly, the persons´ level of education and socioeconomic status were accounted for.
“It seems that the risk for developing dementia after TBI is the highest among middle-aged men. The more severe the TBI, the higher the risk for subsequent dementia. While previous studies have identified good education and high socioeconomic status as protective factors against dementia, we did not discover a similar effect among TBI survivors”. (Rahul Raj, docent of experimental neurosurgery and one of the primary authors of the study) (1). (Source)
Supporting these findings, in a 2015 Univeristy of Edinburg study, scientists have shown that People who have previously experienced severe head or whiplash injuries in the past have been shown to be at greater risk of developing dementia and Alzheimer’s Disease. (2) (Source)
Close to twenty years before these two studies, Researchers had also found that any medical history of head injury more than doubled both the risk of developing Alzheimer’s disease and the chances of developing non-Alzheimer’s dementia, even after adjustment for the effects of age. (3) (Source)
The findings showed that the worse the head injury, the higher the risk of Alzheimer’s disease. Moderate head injury was associated with a 2.3-fold increase in risk, whereas severe head injury more than quadrupled the risk. (4)
The evidence shows that even mild traumatic brain injury can be a significant dementia risk if repetitive, like in American footbal or concussive force of military blasts. Indeed, repetitive mild traumatic brain injury is now recognized as an issue in contact sports, (5) (Source) especially American football as well as the concussive force of military blasts. (5, 6) (Source) Indeed, these violent sport traumas can lead to chronic traumatic encephalopathy (CTE), which is characterized by fibrillar tangles of hyperphosphorylated tau. (Source). (7). High levels of tau protein in fluid bathing the brain are linked to poor recovery after head trauma (8) (Source).
Mechanisms and Tau Proteins
Insofar as pathophysiology is concerned, different mechanisms have been identified. One Research Team has concluded that dementia may be precipitated by an immune reaction (inflammation) that occurs following head injury. Such inflammation can lead to formation of the toxic clumps of the amyloid and tau proteins that are hallmarks of Alzheimer’s disease. (2) (Source)
Given what we know about holistic medicine and lifestyle prevention, it’s reasonable to assume that inappropriate mainstream diets, stress, toxicity (including heavy metals) and other deleterious lifestyle elements may be contributing factors to the TBI-dementia phenomenon.
Top: Neurons were grown in tissue culture and stained with antibody to MAP2 protein in green and MAP tau in red using the immunofluorescence technique. MAP2 is found only in dendrites and perikarya, while tau is found not only in the dendrites and perikarya but also in axons. As a result, axons appear red while the dendrites and perikarya appear yellow, due to superimposition of the red and green signals. DNA is shown in blue using the DAPI stain which highlights the nuclei: image public domain via c.c.
Tau Protein Abnormalities and Hyperphosphorylation
Tau proteins are proteins that stabilize microtubules. They are abundant in neurons of the central nervous system. (9) They are also known as a highly soluble microtubule-associated protein (MAP) (Source). Pathologies of the nervous system such as Alzheimer’s disease and Parkinson’s disease are associated with tau proteins misfolding abnormalities, when they become so defective that they can no longer stabilize microtubules. (10) When misfolded, this otherwise soluble protein can form insoluble aggregates that contribute to a number of neurodegenerative diseases
Traumatic brain injuries can thus promote this misfoldment-based tau dysfunction, one element of which is associated to hyperphosphorylation. (11) Hyperphosphorylation of the tau protein can result in the self-assembly of tangles of paired helical filaments and straight filaments, which are involved in the pathogenesis of Alzheimer’s disease, frontotemporal dementia, and other tau related disorders. (12)
The data shows that hyperphosphorylated tau disassembles microtubules and sequesters normal tau, MAP 1(microtubule associated protein1), MAP 2, and ubiquitin into tangles of PHFs. This insoluble structure damages cytoplasmic functions and interferes with axonal transport, which can lead to cell death and Alzheimers. (13) (Source) Research also suggests that in Alzheimer’s disease, tau may be released extracellularly by an exosome-based mechanism. (14)
Safe and efficient holistic solutions need to be personalized to each Alzheimer’s patient, in particular, each patient needs to be tested so that the clinician can determine what is affecting the brain’s plasticity signaling network. As the Institute’s workshop shows, the following lifestyle elements are essential to kick-start A.D. reversal and tau regularization. 1. Improved Mediterranean Diet and-or improved vegan diet, depending on the patient. 2. Circadian rigor, with deep sleep patterns. 3. Stress management via meditation, yoga and the like. 4. Supplementation: Taking melatonin, methylcobalamin, vitamin D3, fish oil and coenzyme Q10 each day. 5. Optimizing oral hygiene by using an electric flosser and electric toothbrush. 6. Hormonal boosting techniques. 7. Intermittent fasting. By following this core program, the Buck Institute was able to reverse the Alzheimer’s process in 9 out of 10 patients, even those with homozygous and heterozygous ApoE4+. It published its results in 2014 (See the Institute’s Bredensen Protocol page). in 2015, Rush Univeristy carried out a complementary study on a much larger group of elderly people that showed a substantial reduction in Alzheimer’s risk. And from 2012 to 2017, the Happiness Medicine Institute conducted in depth research and some clinical practice that tweaked the “Alzheimer Reversal Code” even further, included, but not limited with special diets, coconut oil, different herbs, essential oils, minerals, (e.g., among others, magnesium) (15) probiotics and berries, in particular the berries that the Institute cultivates at the Mediterranean Holistic rejuvenation Center. (16) (See the Institute’s Workshops and pending ebook on this topic).
Mild traumatic brain injuries are heterogeneous and highly individualized injuries. Recovery and return to pre-injury functioning is influenced by numerous factors. Given the brain’s neuro-plasticity, affected cells can recover and new brain cells can be spurred to grow. The primary pathophysiologies include ionic shifts, abnormal energy metabolism, tau abnormalities, diminished cerebral blood flow, and impaired neurotransmission.
It is important to appreciate that cell death is closely related to injury severity. Mild traumatic brain injuries, especially injuries on the milder end of the spectrum, are typically characterized by cellular dysfunction that is reversible.
However, what distinguishes a TBI that will lead to Alzheimer’s Disease from one that will not depends not only on the severity of the TBI and genetic predisposition, but also on the patient’s age, (17) toxicity level, exercises, diets, sleep pattern, toxicity load and other lifestyle elements. (18) Head injuries are more likely to lead to Alzheimer’s disease in later life if the person has the apolipoprotein E (APOE) gene.
It appears that not enough research has been conducted to see if single head injuries resulting in unconsciousness for less than half an hour pose a definite risk for Alzheimer’s disease or other forms of dementia. But repeated head injuries like in American football, European rugby and boxing have been shown to significantly promote cognitive dysfunction that favor Alzheimer’s, Parkinson’s and other neuro-degenertive diseases.
.As for the Tau question, one of the best Tau hypothesis states that excessive or abnormal phosphorylation of tau results in the transformation of normal adult tau into abnormal PHF-tau (paired helical filament) and NFTs (neurofibrillary tangles). The process of tau aggregation in the absence of mutations does not appear to be presently known. But we hypothesize that it might result from increased phosphorylation, protease action or exposure to polyanions, such as glycosaminoglycans. (19)
“It is a tragedy when an adult of working age develops dementia after recovering from a brain injury, not just for the patient and their families, but it also negatively impacts the whole society. In the future, it will be increasingly important to prevent TBIs and to develop rehabilitation and long-term monitoring for TBI patients,” (PLOS Medicine, 2017; 14 (7))
The WHO has predicted that TBI will become a leading cause of death and long-term illness during the next ten years. Already one per cent of the population in the United States suffers from a long-term disability caused by TBI. And Alzheimer’s Disease now affects close to 50 percent of Americans who reach their 80s. Approximately 5.4 million American patients and 30 million are affected globally (20) In the absence of effective prevention and holistic treatments, by 2050, at least 13 million Americans and 160 million globally will needlessly suffer and die from this disease, burdening even more the Medicare system. Unlike several other chronic illnesses, Alzheimer’s disease prevalence is skyrocketing, which makes the need to develop effective prevention and treatment increasingly pressing. Recent estimates suggest that AD has become the third leading cause of death in the United States, behind cardiovascular disease and cancer. (21) To make matters worse, women are at the epicenter of the Alzheimer’s epidemic, with 65% of AD patients and 60% of caregivers being women (22). Indeed, a woman’s chance of developing AD is now greater than her chance of developing breast cancer. (23)
Those in charge of public policy should thus invest not only in better regulating violent sports, military traumatizing activites, chronic stress, generalized toxicity and, inter alia, processed foods, but the Government should also promote cost-friendly preventive measures and holistic treatment plans via rehabilitation and rejuvenation centers where both TBI and Alzheimer’s patients can start holistic rejuvenation programs that will in the end not only alleviate lots of un-necessary suffering, but also save hundreds of billion of dollars that could be better invested in Life, longevity and prosperity.
Christian Joubert (HMI director and CSO)