This is the first time in the scientific world that non-drug therapy has been proven effective in preventing the core biological processes responsible for the development of Alzheimer's disease.
Using a specific protocol of hyperbaric oxygen therapy (HBOT), cerebral blood flow (CBF) improved/increased in elderly patients by 16-23%, alleviating vascular dysfunction and amyloid burden.
The study from Tel Aviv University, part of a comprehensive research program directed toward aging and accompanying ailments as a reversible disease, holds promise for a new strategic approach to the prevention of Alzheimer's by addressing not only the symptoms or targeting biomarkers, but rather the core pathology and biology responsible for the development of the disease.
Hyperbaric medicine is a form of therapy that requires patients to be kept in special chambers in which the atmospheric pressure is much higher than that normally experienced at sea level.
In addition, they breathe air composed of 100% oxygen.
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Hyperbaric medicine is considered safe and already serves to treat an extensive list of medical conditions. In recent years, scientific evidence has indicated that unique protocols of hyperbaric therapy are capable of inducing repair of damage brain tissue and renewed growth of blood vessels and nerve cells in the brain.
Alzheimer's disease is a neurodegenerative disease that usually starts slowly and progressively worsens. It is the cause of 60–70% of cases of dementia. The most common early symptom is difficulty in remembering recent events. As the disease advances, symptoms can include problems with language, disorientation , mood swings, loss of motivation, self-neglect, and behavioral issues. As a person's condition declines, they often withdraw from family and society. Gradually, bodily functions are lost, ultimately leading to death. Although the speed of progression can vary, the typical life expectancy following diagnosis is three to nine years.
The cause of Alzheimer's disease is poorly understood. There are many environmental and genetic risk factors associated with its development. The strongest genetic risk factor is from an allele of APOE. Other risk factors include a history of head injury, clinical depression, and high blood pressure. The disease process is largely associated with amyloid plaques, neurofibrillary tangles, and loss of neuronal connections in the brain.
A probable diagnosis is based on the history of the illness and cognitive testing with medical imaging and blood tests to rule out other possible causes. Initial symptoms are often mistaken for normal aging. Examination of brain tissue is needed for a definite diagnosis, but this can only take place after death. Good nutrition, physical activity, and engaging socially are known to be of benefit generally in aging, and these may help in reducing the risk of cognitive decline and Alzheimer's; in 2019 clinical trials were underway to look at these possibilities. There are no medications or supplements that have been shown to decrease risk.
No treatments stop or reverse its progression, though some may temporarily improve symptoms. Affected people increasingly rely on others for assistance, often placing a burden on the caregiver. The pressures can include social, psychological, physical, and economic elements. Exercise programs may be beneficial with respect to activities of daily living and can potentially improve outcomes. Behavioral problems or psychosis due to dementia are often treated with antipsychotics, but this is not usually recommended, as there is little benefit and an increased risk of early death.
As of 2015, there were approximately 29.8 million people worldwide with AD with about 50 million of all forms of dementia as of 2020. It most often begins in people over 65 years of age, although up to 10 per cent of cases are early-onset affecting those in their 30's to mid 60's. Women get sick more often than men. It affects about 6% of people 65 years and older. In 2015, all forms of dementia resulted in about 1.9 million deaths. The disease is named after German psychiatrist and pathologist Alois Alzheimer, who first described it in 1906. Alzheimer's financial burden on society is large, on par with the costs of cancer and heart disease, costing 200 billion dollars in the US alone.
Signs and symptoms The course of Alzheimer's is generally described in three stages, with a progressive pattern of cognitive and functional impairment. The three stages are described as early or mild, middle or moderate, and late or severe. The disease is known to target the hippocampus which is associated with memory, and this is responsible for the first symptoms of memory impairment. As the disease progresses so does the degree of memory impairment.
First symptoms The first symptoms are often mistakenly attributed to aging or stress. Detailed neuropsychological testing can reveal mild cognitive difficulties up to eight years before a person fulfills the clinical criteria for diagnosis of Alzheimer's disease. These early symptoms can affect the most complex activities of daily living. The most noticeable deficit is short term memory loss, which shows up as difficulty in remembering recently learned facts and inability to acquire new information.
Subtle problems with the executive functions of attentiveness, planning, flexibility, and abstract thinking, or impairments in semantic memory can also be symptomatic of the early stages of Alzheimer's disease. Apathy and depression can be seen at this stage, with apathy remaining as the most persistent symptom throughout the course of the disease. The preclinical stage of the disease has also been termed mild cognitive impairment . This is often found to be a transitional stage between normal aging and dementia. MCI can present with a variety of symptoms, and when memory loss is the predominant symptom, it is termed amnestic MCI and is frequently seen as a prodromal stage of Alzheimer's disease. Amnestic MCI has a greater than 90% likelihood of being associated with Alzheimer's.
Early stage In people with Alzheimer's disease, the increasing impairment of learning and memory eventually leads to a definitive diagnosis. In a small percentage, difficulties with language, executive functions, perception , or execution of movements are more prominent than memory problems. Alzheimer's disease does not affect all memory capacities equally. Older memories of the person's life , facts learned , and implicit memory are affected to a lesser degree than new facts or memories.
Language problems are mainly characterised by a shrinking vocabulary and decreased word fluency, leading to a general impoverishment of oral and written language. In this stage, the person with Alzheimer's is usually capable of communicating basic ideas adequately. While performing fine motor tasks such as writing, drawing, or dressing, certain movement coordination and planning difficulties may be present, but they are commonly unnoticed. As the disease progresses, people with Alzheimer's disease can often continue to perform many tasks independently, but may need assistance or supervision with the most cognitively demanding activities.
Middle stage Progressive deterioration eventually hinders independence, with subjects being unable to perform most common activities of daily living. Speech difficulties become evident due to an inability to recall vocabulary, which leads to frequent incorrect word substitutions . Reading and writing skills are also progressively lost. Complex motor sequences become less coordinated as time passes and Alzheimer's disease progresses, so the risk of falling increases. During this phase, memory problems worsen, and the person may fail to recognise close relatives. Long-term memory, which was previously intact, becomes impaired.
Behavioral and neuropsychiatric changes become more prevalent. Common manifestations are wandering, irritability and emotional lability, leading to crying, outbursts of unpremeditated aggression, or resistance to caregiving. Sundowning can also appear. Approximately 30% of people with Alzheimer's disease develop illusionary misidentifications and other delusional symptoms. Subjects also lose insight of their disease process and limitations . Urinary incontinence can develop. These symptoms create stress for relatives and carers, which can be reduced by moving the person from home care to other long-term care facilities.
Late stage During the final stage, known as the late-stage or severe stage, the patient is completely dependent upon caregivers. Language is reduced to simple phrases or even single words, eventually leading to complete loss of speech. Despite the loss of verbal language abilities, people can often understand and return emotional signals. Although aggressiveness can still be present, extreme apathy and exhaustion are much more common symptoms. People with Alzheimer's disease will ultimately not be able to perform even the simplest tasks independently; muscle mass and mobility deteriorates to the point where they are bedridden and unable to feed themselves. The cause of death is usually an external factor, such as infection of pressure ulcers or pneumonia, not the disease itself.
Neuropathology Alzheimer's disease is characterised by loss of neurons and synapses in the cerebral cortex and certain subcortical regions. This loss results in gross atrophy of the affected regions, including degeneration in the temporal lobe and parietal lobe, and parts of the frontal cortex and cingulate gyrus. Degeneration is also present in brainstem nuclei particularly the locus coeruleus in the pons. Studies using MRI and PET have documented reductions in the size of specific brain regions in people with Alzheimer's disease as they progressed from mild cognitive impairment to Alzheimer's disease, and in comparison with similar images from healthy older adults.
Both Aß plaques and neurofibrillary tangles are clearly visible by microscopy in brains of those afflicted by Alzheimer's disease, especially in the hippocampus. However, Alzheimer's disease may occur without neurofibrillary tangles in the neocortex. Plaques are dense, mostly insoluble deposits of beta-amyloid peptide and cellular material outside and around neurons. Tangles are aggregates of the microtubule-associated protein tau which has become hyperphosphorylated and accumulate inside the cells themselves. Although many older individuals develop some plaques and tangles as a consequence of aging, the brains of people with Alzheimer's disease have a greater number of them in specific brain regions such as the temporal lobe. Lewy bodies are not rare in the brains of people with Alzheimer's disease.
Diagnosis Alzheimer's disease is usually diagnosed based on the person's medical history, history from relatives, and behavioral observations. The presence of characteristic neurological and neuropsychological features and the absence of alternative conditions is supportive. Advanced medical imaging with computed tomography or magnetic resonance imaging , and with single-photon emission computed tomography or positron emission tomography can be used to help exclude other cerebral pathology or subtypes of dementia. Moreover, it may predict conversion from prodromal stages to Alzheimer's disease. Approved radiopharmaceutical diagnostic agents used in PET for patients with Alzheimer's disease: florbetapir , flutemetamol , florbetaben , flortaucipir .
Assessment of intellectual functioning including memory testing can further characterise the state of the disease. Medical organizations have created diagnostic criteria to ease and standardise the diagnostic process for practising physicians. The diagnosis can be confirmed with very high accuracy post-mortem when brain material is available and can be examined histologically.
Prevention There is no evidence that supports any particular measure as being effective in preventing Alzheimer's disease. Global studies of measures to prevent or delay the onset of Alzheimer's disease have often produced inconsistent results. Epidemiological studies have proposed relationships between certain modifiable factors, such as diet, cardiovascular risk, pharmaceutical products, or intellectual activities, among others, and a population's likelihood of developing Alzheimer's disease. Only further research, including clinical trials, will reveal whether these factors can help to prevent Alzheimer's disease.
Medication Cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes, and smoking, are associated with a higher risk of onset and worsened course of Alzheimer's disease. Blood pressure medications may decrease the risk. A review found that the use of statins, which lower cholesterol may be of benefit in Alzheimer's and other dementias but not in vascular dementia.
Long-term usage of non-steroidal anti-inflammatory drugs were thought in 2007 to be associated with a reduced likelihood of developing Alzheimer's disease. Evidence also suggested the notion that NSAIDs could reduce inflammation related to amyloid plaques, but trials were suspended due to high adverse events. No prevention trial has been completed. They do not appear to be useful as a treatment, but as of 2011 were thought to be candidates as presymptomatic preventives. Hormone replacement therapy in menopause, although previously used, may increase risk of dementia.
Lifestyle Further information: Neurobiological effects of physical exercise Evidence suggests that higher education and occupational attainment, and participation in leisure activities show a reduced risk of developing Alzheimer's, or of delaying the onset of symptoms. This is compatible with the cognitive reserve theory, which states that some life experiences result in more efficient neural functioning providing the individual a cognitive reserve that delays the onset of dementia manifestations. Education delays the onset of Alzheimer's disease syndrome without changing the duration of the disease. Learning a second language even later in life seems to delay the onset of Alzheimer's disease.
Physical exercise is associated with decreased rate of dementia. Physical exercise is also effective in reducing symptom severity in those with Alzheimer's disease.
Diet Diet is seen to be a modifiable risk factor for the development of dementia. The Mediterranean diet, and the DASH diet are both associated with less cognitive decline. A different approach has been to incorporate elements of both of these diets into one known as the MIND diet. These diets are generally low in saturated fats while providing a good source of carbohydrates, mainly those that help stabilize blood sugar and insulin levels. Those who eat a diet high in saturated fats and simple carbohydrates have a higher risk.
Raised blood sugar levels over a long time, can damage nerves and cause memory problems if they are not managed. Nutritional factors associated with the proposed diets for reducing dementia risk, include unsaturated fatty acids, antioxidants vitamin E, vitamin C, and flavonoids, vitamin B, and vitamin D.
The MIND diet may be more protective but further studies are needed. The Mediterranean diet seems to be more protective against Alzheimer's than DASH but there are no consistent findings against dementia in general. The role of olive oil needs further study as it may be one of the most important components in reducing the risk of cognitive decline and dementia.
In those with celiac disease or non-celiac gluten sensitivity, a strict gluten-free diet may relieve the symptoms given a mild cognitive impairment. Once dementia is advanced no evidence suggests that a gluten free diet is useful.
Conclusions on dietary components have been difficult to ascertain as results have differed between population-based studies and randomised controlled trials. There is limited evidence that light to moderate use of alcohol, particularly red wine, is associated with lower risk of Alzheimer's disease. There is tentative evidence that caffeine may be protective. A number of foods high in flavonoids such as cocoa, red wine, and tea may decrease the risk of Alzheimer's disease. A number of studies have looked at the possible role of minerals such as selenium, zinc, and copper. Omega 3 fatty acid supplements from plants and fish, and dietary docosahexaenoic acid , do not appear to benefit people with mild to moderate Alzheimer's disease.
Curcumin as of 2010 had not shown benefit in people even though there is tentative evidence in animals. There is growing evidence for the neuroprotection offered by the use of cannabinoids in Alzheimer's and other neurodegenerative disorders. However, further population studies are recommended to see this use beyond experimental.