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The popular medicine statins could help slow the progression of Alzheimer’s disease, according to a new Swedish study. A number of things can be done to help lower your chances of being diagnosed with Alzheimer’s, including ways in which you can sleep, or even the way you walk….Continue reading….
By: Rudi Kinsella
Source: Irish Star
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Critics:
Alzheimer’s disease accounts for 60–70% of cases of dementia worldwide. The most common symptoms of Alzheimer’s disease are short-term memory loss and word-finding difficulties. Trouble with visuospatial functioning (getting lost often), reasoning, judgment and insight fail. Insight refers to whether or not the person realizes they have memory problems.The part of the brain most affected by Alzheimer’s is the hippocampus.
Other parts that show atrophy (shrinking) include the temporal and parietal lobes. Although this pattern of brain shrinkage suggests Alzheimer’s, it is variable and a brain scan is insufficient for a diagnosis. Little is known about the events that occur during and that actually cause Alzheimer’s disease. This is due to the fact that brain tissue from patients with the disease can only be studied after the person’s death.
However, it is known that one of the first aspects of the disease is a dysfunction in the gene that produces amyloid. Extracellular senile plaques (SPs), consisting of beta-amyloid (Aβ) peptides, and intracellular neurofibrillary tangles (NFTs) that are formed by hyperphosphorylated tau proteins, are two well-established pathological hallmarks of AD. Amyloid causes inflammation around the senile plaques of the brain, and too much build up of this inflammation leads to changes in the brain that cannot be controlled, leading to the symptoms of Alzheimer’s.
Several articles have been published on a possible relationship (as a either primary cause or exacerbation of Alzheimer’s disease) between general anesthesia and Alzheimer’s in specifically the elderly. Vascular dementia accounts for at least 20% of dementia cases, making it the second most common type. It is caused by disease or injury affecting the blood supply to the brain, typically involving a series of mini-strokes.
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 (agnosia), or execution of movements (apraxia) are more prominent than memory problems.
Alzheimer’s disease does not affect all memory capacities equally. Older memories of the person’s life (episodic memory), facts learned (semantic memory), and implicit memory (the memory of the body on how to do things, such as using a fork to eat or how to drink from a glass) 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 (apraxia) 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.
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 (paraphasias).
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 (anosognosia). Urinary incontinence can develop. These symptoms create stress for relatives and caregivers, which can be reduced by moving the person from home care to other long-term care facilities. A normal brain on the left and a late-stage Alzheimer’s brain on the right .During the final stage, known as the late-stage or severe stage, there is complete dependence on 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. In some cases, there is a paradoxical lucidity immediately before death, where there is an unexpected recovery of mental clarity
Alzheimer’s disease is believed to occur when abnormal amounts of amyloid beta (Aβ), accumulating extracellularly as amyloid plaques and tau proteins, or intracellularly as neurofibrillary tangles, form in the brain, affecting neuronal functioning and connectivity, resulting in a progressive loss of brain function.This altered protein clearance ability is age-related, regulated by brain cholesterol, and associated with other neurodegenerative diseases.
The cause for most Alzheimer’s cases is still mostly unknown, except for 1–2% of cases where deterministic genetic differences have been identified. Several competing hypotheses attempt to explain the underlying cause; the most predominant hypothesis is the amyloid beta (Aβ) hypothesis. The oldest hypothesis, on which most drug therapies are based, is the cholinergic hypothesis, which proposes that Alzheimer’s disease is caused by reduced synthesis of the neurotransmitter acetylcholine.
The loss of cholinergic neurons noted in the limbic system and cerebral cortex, is a key feature in the progression of Alzheimer’s.The 1991 amyloid hypothesis postulated that extracellular amyloid beta (Aβ) deposits are the fundamental cause of the disease. Support for this postulate comes from the location of the gene for the amyloid precursor protein (APP) on chromosome 21, together with the fact that people with trisomy 21 (Down syndrome) who have an extra gene copy almost universally exhibit at least the earliest symptoms of Alzheimer’s disease by 40 years of age.
A specific isoform of apolipoprotein, APOE4, is a major genetic risk factor for Alzheimer’s disease. While apolipoproteins enhance the breakdown of beta amyloid, some isoforms are not very effective at this task (such as APOE4), leading to excess amyloid buildup in the brain.
Late-onset Alzheimer’s is about 70% heritable. Genetic models in 2020 predict Alzheimer’s disease with 90% accuracy.
Most cases of Alzheimer’s are not familial, and so they are termed sporadic Alzheimer’s disease.[medical citation needed] Most cases of sporadic Alzheimer’s disease are late onset, developing after the age of 65 years. The strongest genetic risk factor for sporadic Alzheimer’s disease is APOEε4. APOEε4 is one of four alleles of apolipoprotein E (APOE). APOE plays a major role in lipid-binding proteins in lipoprotein particles and the ε4 allele disrupts this function.
Between 40 and 80% of people with Alzheimer’s disease possess at least one APOEε4 allele. The APOEε4 allele increases the risk of the disease by three times in heterozygotes and by 15 times in homozygotes. Like many human diseases, environmental effects and genetic modifiers result in incomplete penetrance. For example, Nigerian Yoruba people do not show the relationship between dose of APOEε4 and incidence or age-of-onset for Alzheimer’s disease seen in other human populations.
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