May 01, · “The fact that prion levels also appear linked to patient longevity should change how we think about the way forward for developing treatments for the disease. We need a sea change in Alzheimer’s disease research, and that is what this paper does. This paper might catalyze a major change in AD research.” What are Prions? Alzheimer's Disease. Caring for a Person with Alzheimer's Disease: Your Easy-to-Use Guide. Get Alzheimer's caregiving information and advice in this comprehensive, easy-to-read guide. Learn caregiving tips, safety information, common medical problems, and how to care for yourself Dec 31, · 1. Introduction. The interest in senile disease is rising gradually because aging society has become a more common phenomenon. Types of dementia include AD, vascular dementia, paralytic dementia, Lewy body dementia, carbon monoxide induced dementia, and trauma dementia [1,2].The onset of AD has continued to increase since , while the prevalence of vascular dementia is
A Review on Studies of Marijuana for Alzheimer’s Disease – Focusing on CBD, THC
Alzheimer's disease AD is a neurodegenerative disease that usually starts slowly and progressively worsens. The cause of Alzheimer's disease is poorly understood. The strongest genetic risk factor is from an allele of APOE, alzheimers disease paper. No treatments stop or reverse its progression, though some may temporarily improve symptoms. As ofthere were approximately The course of Alzheimer's is generally described in three stages, with a progressive pattern of cognitive and functional impairment, alzheimers disease paper.
As the disease progresses so does the degree of memory impairment. The first symptoms are often mistakenly attributed to aging or stress.
Subtle problems with the executive functions of attentivenessplanningflexibility, and abstract thinkingor impairments in semantic memory memory of meanings, and concept relationships can also be symptomatic of the early stages of Alzheimer's disease. MCI can present with a variety of symptoms, and alzheimers disease paper memory loss is the predominant symptom, it is termed amnestic MCI and is frequently seen as a prodromal stage of Alzheimer's disease, alzheimers disease paper.
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, alzheimers disease paper, executive functions, perception agnosiaor execution of movements apraxia are more prominent than memory problems.
Older memories of the person's life episodic memoryfacts learned semantic memoryand 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 fluencyleading to a general impoverishment of oral and written language. Progressive deterioration eventually hinders independence, with subjects being unable to perform most common activities of daily living.
Reading and writing skills are also progressively lost. Behavioral and neuropsychiatric changes become more prevalent. Common manifestations are wanderingirritability and emotional labilityleading to crying, outbursts of unpremeditated aggressionalzheimers disease paper, or resistance to caregiving. During the final stage, known as the late-stage or severe stage, the patient is completely dependent upon caregivers.
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 pneumonianot the disease itself. Alzheimer's disease is believed to occur when abnormal amounts of amyloid betaaccumulating extracellularly as amyloid plaquesalzheimers disease paper, and tau proteinsaccumulating intracellularly as neurofibrillary tanglesform in the brain affecting neuronal functioning and connectivity, resulting in a progressive loss of brain function.
These types are known as early onset familial Alzheimer's diseasealzheimers disease paper, can have a very early onset, and a faster rate of progression.
Most cases of Alzheimer's are not inherited and are termed sporadic Alzheimer's disease, in which environmental and genetic differences may act as risk factors. Most cases of sporadic Alzheimer's disease in contrast to familial Alzheimer's disease are late-onset Alzheimer's disease LOAD developing after the age of 65 years. APOE plays a major role in lipid-binding proteins in lipoprotein particles and the epsilon4 allele disrupts this function.
For example, certain Nigerian populations do not show the relationship between dose of APOEε4 and incidence or age-of-onset for Alzheimer's disease seen in other human populations. Alleles in the TREM2 gene have been associated with a 3 to 5 times higher risk of developing Alzheimer's disease.
Many single-nucleotide polymorphisms SNPs are associated with Alzheimer's, with a study adding 30 SNPs by differentiating Alzheimer's disease into six categories, including memory, language, visuospatial, and executive functioning.
A Japanese pedigree of familial Alzheimer's disease was found to be associated with a deletion mutation of codon of APP. Only homozygotes with this mutation develop Alzheimer's disease. This mutation accelerates Aβ oligomerization but the proteins do not form the amyloid fibrils that aggregate into amyloid plaques, suggesting that it is the Aβ oligomerization rather than the fibrils that may be the cause of this disease.
Mice expressing this mutation have all the usual pathologies of Alzheimer's disease. The oldest hypothesis, on alzheimers disease paper most drug therapies are based, is the cholinergic hypothesis[60] which proposes that Alzheimer's disease is caused by reduced synthesis of the neurotransmitter acetylcholine. The cholinergic hypothesis has not maintained widespread support, largely because medications intended to treat acetylcholine deficiency have not been very effective.
The amyloid hypothesis postulated that extracellular amyloid beta Aβ deposits are the fundamental cause of the disease. While apolipoproteins enhance the breakdown of beta amyloid, some isoforms are not very effective at this task such as APOE4leading to excess amyloid buildup in the brain.
The tau hypothesis proposes that tau protein abnormalities initiate the disease cascade. Eventually, they form neurofibrillary tangles inside nerve cell bodies.
A number of studies connect the misfolded amyloid beta and tau proteins associated with the pathology of Alzheimer's disease, as bringing about oxidative stress that leads to chronic inflammation.
Sleep disturbances are seen as a possible risk factor for inflammation in Alzheimer's disease. Sleep problems have been seen as a consequence of Alzheimer's disease but studies suggest that they may instead be a causal factor, alzheimers disease paper. Sleep disturbances are thought to be linked to persistent inflammation. Cholesterol signaling hypothesis postulates that amyloid production and tau phosphorylation are regulated by cholesterol and high brain cholesterol contributes to the disease, alzheimers disease paper.
First, the cholesterol is made in the astrocytes, the astrocytes load the cholesterol into the cholesterol carrier protein apoEand the apoE loads the cholesterol into the neurons. Once in the neurons, cholesterol causes clustering of amyloid precursor protein APP with its hydrolytic enzyme gamma secretase, resulting in amyloid beta production and accumulation of amyloid plaques. A neurovascular hypothesis stating that poor functioning of the blood—brain barrier may be involved has been alzheimers disease paper. The cellular homeostasis of biometals such as ionic copper, iron, and zinc is disrupted in Alzheimer's disease, though it remains unclear whether this is produced by or causes the changes in proteins, alzheimers disease paper.
These ions affect and are affected by tau, APP, and APOE, [78] and their dysregulation may cause oxidative stress that may contribute to the pathology. Smoking is a significant Alzheimer's disease risk factor. There is tentative evidence that exposure to air pollution may be a contributing factor to the development of Alzheimer's disease.
One hypothesis posits that dysfunction of oligodendrocytes and their associated myelin during aging contributes to axon damage, which then causes amyloid alzheimers disease paper and tau hyper-phosphorylation as a side effect.
Retrogenesis is a medical hypothesis about the development and progress of Alzheimer's disease proposed by Barry Reisberg in the s. The association with celiac disease is unclear, with a study finding no increase in dementia overall in those with CD, while a review found an alzheimers disease paper with several types of dementia including Alzheimer's disease.
Kynurenines are a downstream metabolite of tryptophan and have the potential to be neuroactive. This may be associated with the neuropsychiatric symptoms and cognitive prognosis in mild dementia.
A five-year study focused on the role of kynurenine in Alzheimer's and Lewy body disease and found its increase to be associated with more hallucinations, alzheimers disease paper. Alzheimers disease paper 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, alzheimers disease paper, including degeneration in the temporal lobe and parietal lobeand parts of the frontal cortex and cingulate gyrus. Both Aβ plaques and neurofibrillary tangles are clearly visible by microscopy in brains of those afflicted by Alzheimer's disease, [] especially in the hippocampus. Tangles neurofibrillary 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. Alzheimer's disease has been identified as a protein misfolding diseasea proteopathycaused by the accumulation of abnormally folded amyloid beta protein into amyloid plaques, and tau protein into neurofibrillary tangles in the brain.
Amyloid beta is a fragment from the larger amyloid-beta precursor protein APP a transmembrane protein that penetrates the neuron's membrane.
APP is critical to neuron growth, survival, and post-injury repair. Alzheimer's disease is also considered a tauopathy due to abnormal aggregation of the tau protein. Every neuron has a cytoskeletonan internal support structure partly made up of structures called microtubules.
These microtubules act like tracks, guiding nutrients and molecules from the body of the cell to the ends of the axon and back. A protein called tau stabilises the microtubules when phosphorylatedand is therefore called a microtubule-associated alzheimers disease paper. In Alzheimer's disease, tau undergoes chemical changes, becoming hyperphosphorylated ; it then begins to pair with other threads, creating neurofibrillary tangles and disintegrating the neuron's transport system. Exactly how disturbances of alzheimers disease paper and aggregation of the beta-amyloid peptide give rise to the pathology of Alzheimer's disease is not known.
Accumulation of aggregated amyloid fibrilswhich are believed to be the toxic form of the protein responsible for disrupting the cell's calcium ion homeostasisinduces programmed cell death apoptosis.
Various inflammatory processes and cytokines may also have a role in the pathology of Alzheimer's disease. Inflammation is a general marker of tissue damage in any disease, and may be either secondary to tissue damage in Alzheimer's disease or a marker of an immunological response. Obesity and systemic inflammation may interfere with immunological processes which promote alzheimers disease paper progression.
Alterations in the distribution of different neurotrophic factors and in the expression of their receptors such as the brain-derived neurotrophic factor BDNF have been described in Alzheimer's disease. Alzheimer's disease is usually diagnosed based on the person's medical historyhistory from relatives, and behavioral observations. The presence of characteristic neurological and neuropsychological features and the absence of alternative conditions is supportive. Assessment of intellectual functioning including memory testing can further characterise the state of the disease.
The diagnosis can be confirmed with very high accuracy post-mortem when brain material is available and can be examined histologically. The National Institute of Neurological and Communicative Disorders and Stroke NINCDS and the Alzheimer's Disease and Related Disorders Association ADRDA, now known as the Alzheimer's Association established the most commonly used NINCDS-ADRDA Alzheimer's Criteria for diagnosis in[] extensively updated in A histopathologic confirmation including a microscopic alzheimers disease paper of brain tissue is alzheimers disease paper for a definitive diagnosis.
Good statistical reliability and validity have been shown between the diagnostic alzheimers disease paper and definitive histopathological confirmation. These domains are equivalent to the NINCDS-ADRDA Alzheimer's Criteria as listed in the Diagnostic and Statistical Manual of Mental Disorders DSM-IV-TR published by the American Psychiatric Association.
Neuropsychological tests including cognitive tests such as the Mini—Mental State Examination MMSE are widely used to evaluate the cognitive impairments needed for diagnosis. More comprehensive test arrays are necessary for high alzheimers disease paper of results, particularly in the earliest stages of the disease.
Further neurological examinations are crucial in the differential diagnosis of Alzheimer's disease and other diseases. Caregivers can supply important information on the daily living abilities, alzheimers disease paper, as well as on the decrease, over time, of the person's mental function.
Supplemental testing provides extra information on some features of the disease alzheimers disease paper is used to rule out other diagnoses. Blood tests can identify other causes for dementia than AD [24] —causes which may, in rare cases, be reversible. It is also necessary to rule out delirium, alzheimers disease paper. Psychological tests for depression are employed, since depression can either be concurrent with Alzheimers disease paper disease see Depression of Alzheimer diseasean early sign of cognitive impairment, [] or even the cause.
Due to low accuracy, the C-PIB-PET scan is not recommended to be used as an early alzheimers disease paper tool or for predicting the development of Alzheimer's disease when people show signs of mild cognitive impairment MCI. There is no evidence that supports any particular measure as being effective in preventing Alzheimer's disease, alzheimers disease paper.
Epidemiological studies have proposed relationships between certain modifiable factors, such as diet, alzheimers disease paper, 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.
Cardiovascular risk factors, such as hypercholesterolaemiahypertensionalzheimers disease paper, diabetesand smokingare associated with a higher risk of onset and worsened course of Alzheimer's disease. Long-term usage of non-steroidal anti-inflammatory drugs NSAIDs were thought in to be associated with a reduced likelihood of developing Alzheimer's disease.
Inside Alzheimer’s disease
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September is World Alzheimer's Month, during which time you can get free online access to our latest JAD issue and 20% discount on the print edition of our latest book Alzheimer's Disease and Air Pollution. For more details, click on the visual May 01, · “The fact that prion levels also appear linked to patient longevity should change how we think about the way forward for developing treatments for the disease. We need a sea change in Alzheimer’s disease research, and that is what this paper does. This paper might catalyze a major change in AD research.” What are Prions? Alzheimer's worsens over time. Alzheimer's is a progressive disease, where dementia symptoms gradually worsen over a number of years. In its early stages, memory loss is mild, but with late-stage Alzheimer's, individuals lose the ability to carry on a conversation and respond to their environment
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