Dementia is, by some estimation, the single leading cause of disability. The World Health Organization says one in five people at some point in life will experience dementia. The organization Alzheimer's Disease International says more than 50 million people have dementia worldwide.
Is there really a difference between dementia and just getting old? Yes. Normal healthy aging does not produce a disability that reduces a person’s ability to function in a physical and social environment. If the ability declines to such a point to which the person cannot function, dementia as a geriatric syndrome is established. This happens to a percentage of the population by age 80, but some people live to over 100 and never get dementia.
Clinical dementia results from pathologies affecting the central nervous system. Patients have deficiencies in cognitive functions such as the thinking process, memory, planning, and judgment. Dementia symptoms show up in loss of memory, movement disorders, and changes in the person’s language, judgment, and behavior. Dementia is most common in individuals above the age of sixty-five. Common types include Alzheimer's dementia (the most prevalent type), vascular dementia, Lewy Body dementia, Frontotemporal dementia, and Wernicke-Korsakoff syndrome dementia. The types have different pathological mechanisms.
Vascular dementia results when there is impaired blood circulation to part of the brain: this reduced blood flow is called ischemia. The cause for the impaired circulation may be thrombosis on the major blood vessels or hemorrhage. Hypertension is a risk factor for vascular dementia. Related is Multi-infarct dementia.
A heart attack is more properly called myocardial infarction. A stroke is a called a cerebral infarction: it is injury to brain matter from a stoppage in blood supply - often this stoppage is due to an obstruction in the circulatory system. If the brain cannot get oxygen on a regular basis, it suffers injury and possible long-term loss of function.
Multi-infarct dementia is a loss of cognitive ability that can be attributed to a series of small strokes. One ministroke by itself may not produce a noticeable decline in function, but the combined effects of several strokes results in the person exhibiting symptoms: loss of short-term memory capacity, tendency to wander or get lost, loss of bladder or bowel control, difficulty following instructions.
As with strokes, there is no treatment to reverse brain damage. Medical intervention focuses on reducing the risk of subsequent strokes by addressing serum cholesterol levels, hypertension, diabetes, and other health problems.
Alzheimer's dementia is very common among the elderly and the most common form of dementia. It results when proteins in the form of neurofibrillary tangles accumulate in the brain, resulting in the death of neurons. Alzheimer's kills over 120,000 Americans evey year, and at any time 5 million are thought to be living with this disease. Lewy body dementia can be divided into lewy body dementia proper and Parkinson's dementia. The difference between the two is the timing of when obvious cognitive decline occurs. Both cause movement disorders in the early stages. If the patient suffers a decline in cognitive function within a year, the dementia is called Lewy Body dementia. Past a year and it's called Parkinson's dementia. Experts estimate Dementia with Lewy Bodies makes up 1 in 20 dementia cases, but this estimate may be low because it is difficult to distinguish between Alzheimer's and Lewy Body dementia. Frontotemporal dementia is a neurodegenerative disease affecting the frontal and temporal lobes of the brain. FTD does not affect memory as much as Alzheimer’s in its early stages; the more obvious symptoms are behavioral. As opposed to other types of dementia, frontotemporal dementia happens relatively often in individuals below the age of 65. Finally, Wernicke Korsakoff syndrome results from a deficiency of vitamin B1; this deficiency may be induced by chronic alcoholism.
Creutzfeldt-Jakob dementia. This uncommon disease cannot be predicted as no risk factors have been identified. This condition may be because of stores of irresistible proteins called prions. Creutzfeldt-Jakob can be acquired. Scientists aren’t sure how but protein structures called prions appear to be part of the cause. These prions can be introduced to the body during, say, a cornea transplant. Signs of this lethal condition usually show up after age 60.
Mixed dementia. Post-mortem and autopsy investigations of the cerebrums of individuals 80 years old and older who had dementia show that many had signs of multiple types. A combination of Alzheimer's, Lewy body dementia, and vascular dementia may show up in an individual. Scientists are trying to figure how having blended dementia influences symptoms and what implications it has for choice of treatment.
Huntington's Disease. This hereditary condition causes specific nerve cells in your cerebrum and spinal cord to deteriorate. Signs typically show up around age 30 or 40.
The brain shrinks (undergoes atrophy) as we get old, but this is not necessarily related to dementia. The brain shrinks 10 percent between middle age and age 90.
Traumatic brain injury (TBI). Head injuries afflict boxed, football players, or servicemen as an occupational hazard, and many cases of TBI are from traffic accidents. This condition can cause dementia and parkinsonism. Symptoms may not show up until years after the injury.
The most prevalent type of dementia in the United States is Alzheimer's, making up 70 percent of diagnosed dementia cases. About 7 million Americans have age-related dementia. Experts estimate that one in every six women and one in every ten men past the age of fifty-five years are likely to develop dementia at some point in their lives. Right now it is estimated that 10 percent of people between 80 and 84 have Alzheimer's and 49 percent of those between 90 and 94 (US numbers). The two types of LBD are dementia with Lewy bodies and Parkinson's disease dementia. The difference between the two (for a differential diagnosis) is when the cognitive symptoms start showing up and when movement disorders begin. In its early stages Parkinson's disease dementia makes the patient unable to control his or her movement. Walking is slower and the person may show muscle tremors. Later there are signs of dementia. Dementia with Lewy bodies seems like Alzheimer’s at first with memory loss and personality changes. In the more advanced stages it can cause hallucinations and give the patient involuntary movement or failure to be able to move. Parkinson's is the second most commonmost common neurodegenerative disease. Autopsies often show people had both Alzheimer's and Parkinson’s.
Other than physical injury, the causes of dementia are unknown. There could be multiple causes. Advice for preventing dementia involves physical exercise, brain exercise, and an appropriate diet, but these were all identified via epidemiological studies, not from first principles.
Analysis of brains of people who had Alzheimer’s Disease, and even less severe age-related cognitive decline show (in modern medical imaging) the accumulation of the proteins amyloid and tau in brain tissue. The relationship between cognitive decline and these proteins is not clear. A causal mechanism may exist, but scientists have never shown that.
Atherosclerosis, a bad cholesterol profile, and hypertension are risk factors for dementia. Age is probably the main risk factor and a family history of dementia is also predictive. Scientists have identified genes that are associated with some dementias. Smoking, alcohol use, and diabetes are also factors.
Although dementia is an individual disease, not a herd disease like the flu or measles, some epidemiologists see benefits to approaching dementia in the same way that viral diseases are studied.
Vascular dementia may be caused by cardiovascular disease of some sort. High blood pressure is a risk factor, if not necessarily a direct cause. The cause of Alzheimer’s is unknown and when scientists talk about the origin of that condition they usually talk about plaques in brain tissue. But plaques are a characteristic of the disease, not its cause. Some have speculated that microscopic prions cause Alzheimer’s and maybe Parkinson’s but there is little proof for this hypothesis. At this time the causes are a mystery.
Gum disease? There is evidence of a link between gingivitis and dementia, but the causal mechanism is unknown.
The patient's educational level msy be correlated with incidence of dementia, but any causal mechanism is not understood.
How do we find if someone has it? Doctors use signs, symptoms, and biomarkers to diagnose dementia. Dementia usually produces cognitive decline, and patients will present with memory loss, impaired judgment and thinking, and agnosia, which is an inability to recognize objects previously known to the patient (Duong, Patel & Chang, 2017). An individual may also have apraxia; he or she is not able to perform tasks that were previously routine, such as bathing or even cooking. It is also not uncommon for patients to manifest behavioral and psychological signs in the forms of psychosis, apathy, delusions, and even hallucinations.
Diagnostic tests for dementia include routine laboratory tests to rule out other diseases, brain imaging, and testing for biomarkers. A complete blood count and a comprehensive metabolic panel can give doctors some insight into patient health. A volumetric MRI imaging study on key brain lobes, can look for shrinkage or atrophy - a sign of dementia but not a definitive sign. A standard CT scan or MRI is particularly useful in identifying vascular dementia. Functional imaging tests such as SPECT and PET scans can often identify brain pathologies by looking for metabolic changes (Kumar & Tsao, 2019). PET can find plaques in the brain, but it is known that even people with MCI, but not Alzheimer's, have plaques.
So behavior is really the final deciding factor in diagnosis, and in particulate, the results of tests for cognition is what healthcare professionals look for.
In Alzheimer's dementia, cerebrospinal fluid (CSF) biomarkers can be used for diagnosis. The specific biomarkers are the 42-amino acid A isoform (AB42) and the phosphorylated tau proteins (Zverová, 2018). The biomarkers of Parkinson's disease include oxidative stress-related biomarkers such as Protein DJ-1 and co-enzyme Q10. Alpha synuclein and the neurofibrillary light chai proteins that may abnormally accumulate in the brain are also diagnostic biomarkers of various degenerative types of dementia. Research on the use of diagnostic biomarkers in multiple forms of dementia is, however, still ongoing. The patient’s history and reports from friends, family, or caregivers are important, too. Testimony from the patient about his or her subjective experience is also factored into a doctor’s diagnosis.
In 2020 a blood test for a biomarker of Alzheimer's was introduced but it was not approved by the FDA.
After death, autopsy can find if a person had Alzheimer's. Postmortem analysis shows plaques (amyloid) and tangles (tau) in brain tissue.
Most individuals living with dementia are past the age of sixty-five and have many associated comorbidities. Epidemiologists estimate that on average, such individuals have four chronic diseases besides dementia; common comorbidities include diabetes, hypertension, musculoskeletal disorders, and chronic cardiac conditions such as heart failure.
Diabetes due to uncontrolled blood sugar levels puts patients at an increased risk of microvascular and macrovascular complications. Hypertension, on the other hand, results due to uncontrolled blood pressure exposes older individuals to the risk of hemorrhagic cerebrovascular accidents from the rupture of the blood vessels.
How do doctors know if someone has dementia? How do they distinguish different tyoes of dementia?
Dementia has no easy biomarkers. Doctors can’t analyze blood and find a hallmark of dementia. It is diagnosed by observation of patient behavior. Post-death autopsies can help identify the cause of the dementia - e.g. lewy bodies in the brain for Lewy Body dementia and plaques for Alzheimer’s.
Is dementia reversible? Can it be cured?
In most cases, no. There are cases of vascular dementia for which improvements in blood flow have partially reversed the dementia, but Alzheimers and Lewy Body Dementia, the most common types, cannot be cured or reversed. Drug therapy may be able to retard the progression of the dementia symptoms, but they do not generally recede.
I heard people with brain cancer can get dementia.
That's right.Do people with dementia sometimes come out of it for a short period?
Some demenetia patients spontaneously appear to lose their dementia, at least for a short time, in something called paradroxial lucidity. Paradoxical Lucidity, or Terminal Lucidity, is a phenomenon that has been described in medical literature for almost a century but is yet to be explained. Understanding the mechanism behind Paradoxical Lucidity could radically change treatment of dementia and other neurological phenomena.
The pharmaceutical companies have spent a lot of effort to address demetia, but have little to show for it. Clinical trials of candidate drugs have been unsuccessful. Drugs in use only target symptoms, not causes. Roughly, there are two types of drugs:
Most treatments affect only symptoms; cognitive decline continues.
Aducanumab is a drug developed by Biogen for Alzheimer’s Disease and approved by the FDA in June 2021. Biogen had disappointing results a few years ago and the company announced it would stop development. But new results were positive and the company applied for approval. The pervious last new Alzheimer’s was approved in 2003. Aducanumab is thought to attack the plaques that accumulate in the brain. Other drugs only reduce the symptoms. The FDA approval was controversial with experts going on record stating they did not think the evidence merited approval.
People with a good cognitive reserve seem better able to cope with dementia. Cognitive reserve is the multiple ways a person's brain works, so that if some paths are closed off from dementia, the person's thinking and memory is resiliant.
Infectious diseases occur when pathogens get inside the body. Animal to human disease is infectious but not contagious. Contagious diseases are infectious diseases that spread from person to person. Infectiousness refers to how many bacteria, pathogens, etc are needed to infect.
The prevailing wisdom is that disease of old age (heart disease, cancer, diabetes, dementia) are not caused by infections and are not a contagion risk to anyone. However, some scientists suspect that these diseases may in fact be caused - or partially caused - by unknown viruses or other agents.
Prions, which were discovered in the 1980s, have been implicated in diseases of the nervous system, even if the mechanism is not understood. There is informed speculation - unproven yet - that prions may cause Alzheimer’s. And further, that prions pass from person to person and that Alzheimer’s is therefore transmissible. Casual contact is still thought to not cause prion transmission, but medical procedures in which a metal instrument enters the body of someone with Alzheimer’s prions (even if the disease has not manifested itself) could be a transfer channel if the instruments are later used on another patient. Prions are known to stick to stainless steel and conventional sterilization methods may be inadequate to prevent prion transfer. This is still speculative, but it is intriguing.
Optical equipment may be a possible path for transmission. People with prion diseases get prions in their eyes even before they show symptoms of the disease. One worry is that people with these prions get eye exams, and the opthalmological equipment becomes contaminated with prions. Even though the equipment is cleaned, the prions may be left on the surface and the next person who is examined with that equipment may acquire the prions and hence, years in the future, the disease.
There is also the idea that amyloid protein clumps characteristics of Alzheimer's could be like prions and self-replicate. And that these could travel from person to person and be a vehicle of disease transmission. Human growth hormone taken from the pituitary glands of cadavers could be a way amyloid beta proteins get into a new person.
There's no guaranteed method to prevent or forestall dementia; however, there are steps one can take that may help.
Duong, S., Patel, T., & Chang, F. (2017). Dementia: What pharmacists need to know. Canadian pharmacists journal : CPJ = Revue des pharmaciens du Canada : RPC, 150(2), 118–129. doi:10.1177/1715163517690745. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5384525/
HealthyPeople, (2019). Dementias, Including Alzheimer’s Disease. Retrieved from: https://www.healthypeople.gov/2020/topics-objectives/topic/dementias-including-alzheimers-disease
Hills, K. (2019). Dementia Statistics- U.S. & Worldwide Stats. Retrieved from: https://braintest.com/dementia-stats-u-s-worldwide/
Kumar, A., & Tsao, J.W. (2019). Alzheimer Disease. Treasure Island: StatPearls Publishing. Retrieved from: https://www.ncbi.nlm.nih.gov/books/NBK499922/
Zverová M. (2018). Alzheimer's disease and blood-based biomarkers - potential contexts of use. Neuropsychiatric disease and treatment, 14, 1877–1882. doi:10.2147/NDT.S172285. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6055879/