Alzheimer’s is also caused by genetic mutations; close relatives have of a four times greater chance of developing the disease. As a rule, Alzheimer’s develops earlier in patients for whom the disease is genetic; symptoms mostly appear well before the age of 65, but sometimes as early as 50. However, just because someone has the mutated gene does not automatically mean that they will develop the disease, which is why preventative genetic tests are inconclusive. As a rule, variations of the gene ApoE, Presenilin-1, -2 and APP are responsible for an early accumulation of β-Amyloid-Peptide.

Over the course of the disease, neurons die off, causing the brain mass to decrease. This creates the expansion of chambers, ventricals and gyri. In addition, the neurotransmitter acetylcholine is no longer produced in sufficient amounts and the synapses (transfer points) die off, limiting the transfer of information in the brain. These changes in the brain tissue lead to a loss of memory and orientation, as well as to a reduction in the patient’s ability to think and feel (lt. Bib. 1). Next, short-term memory begins to fail: things that have recently been absorbed by the brain are forgotten and things that are rarely used are lost. However, long-term memory continues to function: positive or negative memories that are linked to strong emotions are not affected. For this reason, a person with Alzheimer’s can recall every detail of the war or other events in the distant past.The Hippocampus is the central coordinator for the transfer of contents from the short-term to the long-term memories. Because Alzheimer’s has damaged this region, no new information can be transferred; however the information that was available before the disease took over is still available.

 

An additional symptom of Alzheimer’s disease is the tendency to have unpredictable emotional outbursts. The reason for this is that the hippocampus is a part of the limbic system, which processes emotional stimuli. The decomposition of cells in this area causes emotions to no longer be controllable.

In advanced stages of the disease, Alzheimer’s patients are often no longer able to perform difficult motor skills (for example, knitting), which is controlled by the thalamus.

One reason for the changes in the cells of Alzheimer’s patients may be the hyperphosphorylated tau protein, which accumulates in the cells in the form of neurofibrillary tangles, blocking the cellsand causing them to die. A further cause may be senile plaques. They consist of β-amyloids and are deposited on to neurons, which inhibit their supplyand activities. Senile plaques can also developwhen the enzyme BACE1 cuts the APP (amyloid beta precursor protein). This results in an abnormally folded β-amyloid, which then deposits in forms of dense formations on the neurons in the brain and causes them to die.

In healthy human brains, there is a balance between BACE1 and the regulating microRNA 107. microRNA 107 is able to block the synthesis of BACE1, therefore limiting the development of β-amyloids. In Alzheimer’s patients, there is an imbalance: due to a lack of microRNA 107, the enzyme BACE1 takes the upper hand and causes a massive formation of senile plaques (Wang). With this “mixed ratio,” we began our laboratory work.