Alzheimer’s Disease: Effects on the Human Brain

Alzheimer’s disease is an irreversible, progressive neurological disorder that impairs thinking and memory. Symptoms include short-term memory loss, poor thinking ability, and changes in temperament. Prevalence is estimated to be around 46.8 million, with 1 in 85 individuals affected by 2050. Prevention/treatment includes regular exercise, social engagement, dietary modifications, mental stimulation, stress management, quality sleep, and caregiving. Causes include genetic factors, buildup of amyloid precursor proteins, and abnormalities in tau protein.

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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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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