Alzheimer's Disease: A Comprehensive Report on Causes and Treatment

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This report provides a comprehensive overview of Alzheimer's disease, an irreversible neurological disorder characterized by progressive impairment of thinking and memory, typically appearing after age 60. It delves into the disease's features, including short-term memory loss, poor thinking ability, and changes in temperament. The report explores the causes, such as genetic factors (APOE gene, mutations in APP and presenilin genes), neurotransmitter deficiencies (acetylcholine), and the formation of neurofibrillary tangles. It also discusses risk factors like smoking, alcoholism, hypertension, and lifestyle choices. Furthermore, the report highlights potential treatments and preventative measures, including acetylcholinesterase inhibitors, NMDA receptor antagonists, regular exercise, dietary modifications, mental stimulation, and caregiving strategies. The report also provides prevalence estimates and implications of the disease.
Document Page
Alzheimer’s diseases refers to an irreversible, progressive
neurological disorder that results in an impairment in thinking and
memory. The symptoms generally appear after 60 years of age.
The goal of the research was to investigate the effects of the
disease on the human brain
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symptoms in Alzheimer's disease: past progress and anticipation of the future. Alzheimer's & dementia: the journal of the
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Abstract
Prevalence
Risk factors
Implications
Short-term memory loss
Difficulty to remember recent information
Poor thinking ability
Speaking problems, low verbal fluency and lexical retrieval
problems
Repeating conversations (Geda et al., 2013)
Changes in temperament and personality
Loss of interest in activities
Isolation and social withdrawal
DisorientationThe number of people suffering from dementia is
estimated to be around 46.8 million. The worldwide
prevalence of Alzheimer’s disease was 26.6 million in
the year 2006. Estimates suggest that the prevalence
will be as high as 1 in 85 individuals, by the year 2050
(Brookmeyer et al., 2007).
References
Prevention/Treatment
Regular exercise- Combination of cardiovascular and muscle
strengthening exercise such as, swimming and walking
Social engagement
Dieatary modifications- cutting down sugar, avoiding trans fat
and eating food rich in omega-3 fats
Mental stimulation
Stress management
Quality sleep
Care giving- Use of feeding tubes, labeling household items,
lifestyle modifications, hygiene maintenance.
Acetylcholinesterase inhibitors (donepezil, galantamine,
rivastigmine, tacrine)- They increase the amount of acetylcholine
in the brain by reducing its breakdown (Benzinger et al., 2013).
NMDA receptor antagonist (memantine)- Deactivates the NMDA
receptors, thereby blocking transfer of electrical impulses
between brain and spinal cord.
Cause
Smoking and alcoholism
Hypertension
Diabetes
High cholesterol
Sedentary lifestyle
Obesity
Depression Figure three
Genetic- 0.1% I AD is inherited in an autosomal
dominant manner. Apolipoprotein E (APOE) is the
best known genetic risk factor.
Buildup of amyloid precursor proteins and presenilin
1 and 2 are thought to be responsible for incidence
of AD.
Mutations in the APP and presenilin genes lead to
formation of senile plaques (amyloid beta deposits)
(Drachman, 2014).
Reduction in synthesis of acetylcholine
neurotransmitter results in AD.
Abnormalities in hyperphosphorylated tau protein
results in formation of neurofibrillary tangles that
disintegrate the microtubule and cytoskeleton
(Martin et al., 2013).
Loss of neurons and synapses from the cerebral cortex and
subcortical regions. Atrophy of affected brain regions and
brainstem degeneration
Degeneration of the parietal and temporal lobe, portions of
cingulate gyrus and frontal cortex (Brookmeyer et al., 2007).
ALZHEIMER’S DISEASE
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Features
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