Most Common Form Of Dementia Biology Essay

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Alzheimers disease is the most common form of dementia that accounts for 50 to 70 percent of dementia cases. The word dementia is used to describe the symptoms like loss of memory, mood changes, and problems with communication and reasoning that occur when the brain is damaged or affected by certain condition or disease including Alzheimer's. The messages in brain disrupted and the connections between the brain cells are damaged due to the shrinking of brain cells. This is because an abnormal material builds up as "tangles" in the centre of the cells and "plaques" form outside the cells. Hence, the information cannot be recalled or assimilated. This is how it's affects certain functions and abilities progressively. ( The highest risk factor for Alzheimer's is increasing age and majority of people with the disease is over 65 years old. However, Alzheimer's is not a normal part of aging. This is because over than 5 percent people with the disease have early onset Alzheimer's (also known as younger-onset), which frequently appears when someone is in their age of 40s or 50s. Alzheimer's is a progressive disease. The symptoms of dementia will become gradually worsen over time. Hence, there is no cure for the disease but there is treatment for dementia symptoms that can temporarily slow down the worsening of dementia symptoms. (


The causes for Alzheimer's disease are idiopathic. However, there are some factors that may cause the Alzheimer's disease such as aging, environmental factors, genetic inheritance, lifestyle and overall general health. There are also some additional factors that may causes Alzheimer's disease like cerebral hypoxia (insufficient supply of oxygen to the brain), head trauma, herpes simplex encephalitis (HSE: a devastating human disease caused by Herpes simplex virus), hysteria, seizures, Wernicke-Korsakoff syndrome (a brain disorder due to lack of thiamine/ vitamin B1), drugs, electroconvulsive therapy (a treatment for severe depression) and temporal lobe surgery. (


Amyloid -Peptide

The major protein in neuritic plaques is amyloid -peptide (A), which is proteolytically derived from a membrane protein, the -amyloid precursor protein (APP) encoded by a gene on chromosome 21q21.3-22.05. APP interacts with extracellular matrix and supports the growth of neurites in neuronal cultures. Genetic evidence implicates A in the pathogenesis of Alzheimer's disease. Almost all patients with trisomy 21 (Down syndrome) develop pathologic changes indistinguishable from those seen in Alzheimer's disease, suggesting that having an increased copy of the APP gene increases the metabolism of APP to A. About 10% of cases of Alzheimer's disease are familial, with early onset (before age 65 years) and autosomal dominant inheritance. In approximately 5% of these families, Alzheimer's disease is strongly linked to missense mutations immediately flanking the A sequence in the APP gene. Transgenic mice expressing human APP with these mutations show elevated levels of A, behavioral abnormalities, and neuritic plaques. The APP mutations result in either increased production of all forms of A or mainly in the long 42-amino-acid form, A42, which self-aggregates and promotes plaque formation. A is toxic to cultured neurons and stimulates production of cytokines from microglial cells. A also triggers the release of glutamate from glial cells and may injure neurons through excitotoxicity. This evidence links increased production of A, particularly A42, to Alzheimer's disease and suggests that A causes the neurodegeneration. Transgenic mice that express mutant forms of familial human APP develop synaptic dysfunction before plaque deposition, indicating that diffusible forms of A are neurotoxic. This may explain why plaque number and disease severity correlate poorly.


The enzymatic pathways that regulate A formation are critical areas of current research that may lead to new treatments. Some clues have come from analysis of additional families with Alzheimer's disease. APP is cleaved at the amino terminal of the A sequence by the membrane-anchored protease BACE, or beta-amyloid precursor protein cleaving enzyme, which is also known as beta-secretase. This cleavage generates a 99-amino-acid carboxyl terminal fragment. A second enzymatic activity termed -secretase cleaves this fragment to yield A. Almost 70% of familial cases of Alzheimer's disease have been linked to missense mutations in the gene PS-1/S182, which encodes a seven-trans-membrane protein (presenilin 1) on chromosome 14q24.3. Another 20% of cases have been linked to mutations in another gene, STM2 (presenilin 2), on chromosome 1q31-42. The proteins encoded by these genes are 67% identical in amino acid sequence and presumably have similar functions. Current evidence indicates that the presenilins are subunits of -secretase, because mutant mice lacking either presenilin show reduced -secretase function, and mutations designed to inhibit the predicted aspartyl protease function of presenilins eliminate -secretase activity. Mutant variants of presenilins associated with familial Alzheimer's disease increase the production of A42. This suggests that these mutations produce Alzheimer's disease by selectively altering -secretase activity to favor production of the longer, amyloid-producing form of A. In addition, -secretase is important for processing Notch proteins and other substrates critical for neuronal function, and mice deficient in presenilins show deficiencies in spatial memory and synaptic plasticity. Thus, -secretase deficiency may contribute to neurodegeneration in patients with presenilin mutations.

Apolipoprotein E

The majority of patients with Alzheimer's disease are older than 60 years, and in about 50% of these patients the e4 isoform of apolipoprotein E (apoE4) has been identified as a risk factor. ApoE is a 34-kDa protein that mediates the binding of lipoproteins to the low-density lipoprotein (LDL) receptor and the LDL receptor-related protein (LRP). It is synthesized and secreted by astrocytes and macrophages and is thought to be important for mobilizing lipids during normal development of the nervous system and during regeneration of peripheral nerves after injury. There are three major isoforms (apoE2, apoE3, and apoE4), which arise from different alleles (e2, e3, and e4) of a single gene on chromosome 19q13.2. The e3 allele is the most common, accounting for about 75% of all alleles, whereas e2 and e4 account for roughly 10% and 15%, respectively. The e4 allele is associated with increased risk and earlier onset of both familial and sporadic late-onset Alzheimer's disease. In contrast, inheritance of e2 is associated with decreased risk and later onset. It is important to note that Alzheimer's disease develops in the absence of e4 and also that many persons with e4 escape disease. Therefore, genotyping is not currently recommended as a useful genetic test.

The mechanism by which apoE alleles alter disease risk is not certain. In cultured neurons, apoE3 increases neurite outgrowth in the presence of very low-density lipoproteins, whereas apoE4 inhibits outgrowth. Alzheimer patients who are homozygous for the e4 allele have larger and denser senile plaques than patients homozygous for the e3 allele. ApoE is found in neuritic plaques, and apoE4 binds A more readily than does apoE3. Therefore, apoE4 may facilitate plaque formation or reduce the clearance of A from brain tissue. In addition, apoE enters neurons and binds the microtubule-associated protein tau, which is the major constituent of neurofibrillary tangles. ApoE3 binds tau much more avidly than apoE4. Binding of apoE3 to tau may prevent the formation of neurofibrillary tangles and support normal microtubule assembly required for neurite outgrowth. (McPhee and Hammer, 2010)

Signs and Symptoms

It is difficult to differentiate between the first signs of Alzheimer's disease and age-related changes. There are ten early signs for Alzheimer's that need to be aware of.

1st: Memory loss that affect daily life

It is the most common sign of Alzheimer's especially in early stages. Compared to age-related changes, sometimes they will forget names and appointments but remembering them later on. In Alzheimer's disease, they often forget any recently learned information, important dates or events, and increasingly need to rely on memory aides such as reminder or family members for things they used to handle on their own.

2nd: Changes in problems solving and planning

People who normally balance their checkbooks may be momentarily disconcerted when the task is more complicated than usual, but will eventually figure out the solution. Someone with Alzheimer's disease could forget completely what the numbers are and what needs to be done with them.

3rd: Difficulty performing familiar task

Busy people can be distracted from time to time and leave the carrots on the stove, only remembering to serve them at the end of the meal. People with Alzheimer's disease could prepare a meal, forget to serve it, and even forget they made it.

4th: Disorientation of time and place

It's normal to forget the day of the week or your destination for a moment. But people with Alzheimer's disease can become lost on their own street or in a familiar shopping mall, not knowing where they are, how they got there or how to get home.

5th: Problems with abstract thinking

People who normally balance their checkbooks may be momentarily disconcerted when the task is more complicated than usual, but will eventually figure out the solution. Someone with Alzheimer's disease could forget completely what the numbers are and what needs to be done with them.

6th: Problems with language

Everyone has trouble finding the right word sometimes, but can finish the sentence with another appropriate word. A person with Alzheimer's disease may forget simple words, or substitute inappropriate words, making their sentence incomprehensible.

7th: Misplacing things

Anyone can misplace their wallet or keys, but eventually find them by reconstructing where they could have left them. A person with Alzheimer's disease may put things down in inappropriate places - an iron in the freezer, or a wristwatch in the sugar bowl - and not be able to retrieve them.

8th: Poor or decreased judgment

People can become so immersed in an activity or telephone conversation they temporarily forget the child they're watching. A person with Alzheimer's disease could entirely forget the child under their care and leave the house to visit a neighbor.

9th: Loss of Initiative

It's normal to tire of housework, business activities or social obligations, but most people regain their initiative. The person with Alzheimer's disease may become very passive and require cues and prompting to get them involved in activities.

10th: Changes in mood or personality

Everyone has a bad day once in a while, or may become sad or moody from time to time. Someone with Alzheimer's disease can exhibit rapid mood swings for no apparent reason: e.g. from calm to tears to anger to calm in a few minutes. People's personalities ordinarily change somewhat at different ages, as character traits strengthen or mellow. But a person with Alzheimer's disease can change drastically, becoming extremely irritable, suspicious or fearful.

Alzheimer's disease is known as a progressive fatal illness where the brain functions will decline gradually when the age increase. It is hard to classify the specific stages of symptoms for patients with Alzheimer's by observation. Most patients with the disease progress through a series of stages (Hill, 2008). They are not uniform in every patient and the stages usually overlap. Symptoms seem to progress in a recognizable pattern and these stages provide a framework for the study of the disease. The following stages of symptoms are outline by Gwyther (1985) from American Health Care Association and Alzheimer's disease and Related Disorders Association:

1st Stage:  2 - 4 years leading up to and including diagnosis:


Recent Memory loss begins to affect job performance

Confusion about places - gets lost on way to work.

Loses spontaneity, becomes withdrawn, disinterested

Mood/personality changes - becomes anxious about symptoms, avoids people.

Poor judgment - makes bad decisions.

Takes longer with routine chores

Trouble handling money, paying bills.


Forgets which bills are paid and phone numbers that are called frequently.

Loses things.  Forgets grocery list.

Arrives at wrong time or place, or constantly rechecks calendar or clock.


2nd Stage:  2 - 10 years after diagnosis (longest stage):


Increasing memory loss and confusion - shorter attention span.

Problems recognizing close friends and/or family.

Repetitive statements and/or movements.

Restless, especially in late afternoon and at night.

Occasional muscle twitches or jerking.

Perceptual-motor problems

Difficulty organizing thoughts, or thinking logically.

Can't find right words - makes up stories to fill in the blanks.

Problems with reading, writing, and numbers.

May be suspicious, irritable, fidgety, teary, or silly.

Loss of impulse control - sloppy - won't bathe or afraid to bathe - trouble dressing.

Gains and then loses weight.

May see or hear things that are not there.

Needs full-time supervision.


Can't remember visits even though the visitor just left.

Mixes up day and night, may get up and wander.

Difficulty getting into a chair, setting the table for a meal.

Can't follow written signs, write name, add or subtract.

May accuse spouse of hiding things, infidelity, or childish behavior.

May undress at inappropriate times or in wrong place.

Forgets when last meal was eaten, may gradually lose interest in food.

3rd/Terminal Stage:  1 - 3 years


Can't recognize family or self in mirror.

Loses weight even with good diet.

Little capacity for self care.  Can't communicate with words.

May put anything in mouth or touch anything.

Can't control bowels or bladder

May have seizures, experience difficulty with swallowing, skin infections.


Looks in mirror and talks to own image.

Needs total care with bathing, dressing, eating and toileting

May groan, scream or make grunting noises.

Sleeps more, becomes comatose, and eventually dies.