Introduction
Alzheimer’s disease (AD) is a complex, irreversible brain disorder that causes nerve cells to die within the brain, progressively affecting dysfunction in memory and cognitive ability, behaviour and language problems (National Institute on Aging, n.d.). Primarily this disease affects older adults over the age of sixty, although it is not considered a normal part of the aging process (Dementia Alliance International, n.d.). AD is considered the most common of the dementia diseases, a medical term that best describes a cluster of disorders involving the deterioration of the brain, (Miller, 2012, p. 252). It accounts for 60-70% of the one hundred different diseases that encompass the dementia umbrella (Australian Institute of Health …show more content…
With age being the most common risk factor, associating with familial disorders and environmental factors, genes alone do not instigate the disease. The human body contains twenty-three chromosome pairs, of which four can be linked to AD (Miller, 2012, pp.254-55). Familial Alzheimer’s disease (FAD), affects less than 1% between the age of thirty and sixty years (Blennow, de Leon & Zetterberg, 2006). In fact, the early onset disease has a 50% inheritance pattern, where, indirectly pathogenic gene mutations lead into development of AD. The genes presenilin 1 on chromosome 14, presenilin 2 mutation on chromosome 1 and the rarer form, abnormalities of the amyloid precursor protein gene (APP) on chromosome 21 genes (Alzheimer’s Australia, …show more content…
Very severe cognitive decline (severe or end-stage ad, e.g., loss of ability to communicate, ambulate & interact).
(Miller, 2012, p.258)
Management
There is no solid treatment per se, but management regimes and interventions. In Australia, there are four drugs that are approved by the Therapeutic Goods Administration (TGA) for AD. Donepezil (Aricept), Rivastigmine (Exelon) and Galantamine (Reminyl) all work similarly by preventing the breakdown of acetylcholine in the brain, allowing for better neural function via concentration of the neurotransmitter. The outcome is a reduction in cognitive and neuropsychiatric symptoms, making early detection the key factor in maximize drug efficacy (Ramachandran, Dhanaraju & Sanjay, 2013, p.1.).
Memantine, a N-methyl-D-aspartate (NMDA) receptor antagonist drug, blocks glutamate (an excitory neurotransmitter) in the brain. Memantine targets moderate to severe AD patients, but not all AD patients are suitable for the drug (MIMS online, 2016). Alternatively, symptoms can be treated individually.
Alternatively, management of symptoms with Non Pharmacological Approaches can be just as effective, but is subjective to the person.
. Cognitive Behavioural Therapy - useful at the time of initial
Alzheimer’s disease (AD) is a complex, irreversible brain disorder that causes nerve cells to die within the brain, progressively affecting dysfunction in memory and cognitive ability, behaviour and language problems (National Institute on Aging, n.d.). Primarily this disease affects older adults over the age of sixty, although it is not considered a normal part of the aging process (Dementia Alliance International, n.d.). AD is considered the most common of the dementia diseases, a medical term that best describes a cluster of disorders involving the deterioration of the brain, (Miller, 2012, p. 252). It accounts for 60-70% of the one hundred different diseases that encompass the dementia umbrella (Australian Institute of Health …show more content…
With age being the most common risk factor, associating with familial disorders and environmental factors, genes alone do not instigate the disease. The human body contains twenty-three chromosome pairs, of which four can be linked to AD (Miller, 2012, pp.254-55). Familial Alzheimer’s disease (FAD), affects less than 1% between the age of thirty and sixty years (Blennow, de Leon & Zetterberg, 2006). In fact, the early onset disease has a 50% inheritance pattern, where, indirectly pathogenic gene mutations lead into development of AD. The genes presenilin 1 on chromosome 14, presenilin 2 mutation on chromosome 1 and the rarer form, abnormalities of the amyloid precursor protein gene (APP) on chromosome 21 genes (Alzheimer’s Australia, …show more content…
Very severe cognitive decline (severe or end-stage ad, e.g., loss of ability to communicate, ambulate & interact).
(Miller, 2012, p.258)
Management
There is no solid treatment per se, but management regimes and interventions. In Australia, there are four drugs that are approved by the Therapeutic Goods Administration (TGA) for AD. Donepezil (Aricept), Rivastigmine (Exelon) and Galantamine (Reminyl) all work similarly by preventing the breakdown of acetylcholine in the brain, allowing for better neural function via concentration of the neurotransmitter. The outcome is a reduction in cognitive and neuropsychiatric symptoms, making early detection the key factor in maximize drug efficacy (Ramachandran, Dhanaraju & Sanjay, 2013, p.1.).
Memantine, a N-methyl-D-aspartate (NMDA) receptor antagonist drug, blocks glutamate (an excitory neurotransmitter) in the brain. Memantine targets moderate to severe AD patients, but not all AD patients are suitable for the drug (MIMS online, 2016). Alternatively, symptoms can be treated individually.
Alternatively, management of symptoms with Non Pharmacological Approaches can be just as effective, but is subjective to the person.
. Cognitive Behavioural Therapy - useful at the time of initial