Alzheimer's disease


Alzheimer's is a type of dementia that causes problems with memory, thinking and behavior. It is a brain disease; amyloid plaques accumulate between nerve cells and brain tissue shrink.


Brain disease

While Alzheimer's increases, brain tissue shrinks. In addition, the brain cavities (ventricles) are remarkably higher. In the early stages of Alzheimer's disease, short-term memory begins to go down as the cells in the hippocampus, degenerate reverse. This increases the ability to perform everyday routine tasks.

As Alzheimer's disease spreads through the outer layer of the cerebral cortex of brains, it can result in reduced understanding, emotional outbursts, and impaired speech. Later, as more nerve cells die, behavioral changes as wandering and agitation start. Ultimately, the ability to recognize faces and to communicate disappears.

Symptoms usually develop slowly and get worse over time, becoming severe enough to interfere with daily tasks. The symptoms of Alzheimer's appear initially to 'normal' aging. The memory loss is much more severe and progressive in nature. The symptoms are:

changes in personality,
disorientation and loss of speech.


Innocent beginning
Alzheimer's disease often begins "innocent" with the first symptoms: mild memory loss and declining responsiveness due to reduced brain activity. These are just some of the early symptoms of this brain disorder, which mainly manifests in individuals aged 65 years and older. The rate at which Alzheimer's develops varies with each patient.


Three stages (some mention seven stages)

In three successive stages a characteristic deterioration of mental and physical condition of the patient can be observed. The duration of the disease is an average of seven years.

  1. reduced understanding, emotional outbursts, and impaired speech
  2. behavioral changes as wandering and agitation
  3. disappearing ability to recognize faces and to communicate

Learn more...:Thanks to : Alzheimer's Association:

Picture above: Notice the big 'holes' in the brains, especially the locations where the memory is situated.

Picture below: accumulation of amyloid plaques between nerve cells in the brain


One of the hallmarks of Alzheimer's disease is the accumulation of amyloid plaques (amyloidosis) between the nerve cells in the brains. Normally amyloid (protein) plays a role in the growth of nerve cells and the repair of these nerve cells.

Under some circumstances, something goes wrong and they are sticky substances, and trapped in the nerve cells. Whether that is the cause of Alzheimer's disease or the result is still uncertain.

Two abnormal structures called plaques and tangles are prime suspects in damaging and killing nerve cells.

Plaques are deposits of a protein fragment called beta-amyloid that build up in the spaces between nerve cells.

Tangles are twisted fibers of another protein called tau that build up inside cells.

Though most people develop some plaques and tangles as they age, those with Alzheimer's tend to develop far more. They also tend to develop them in a predictable pattern, beginning in areas important for memory before spreading to other regions.

Scientists do not know exactly what role plaques and tangles play in Alzheimer's disease. Most experts believe they somehow play a critical role in blocking communication among nerve cells and disrupting processes that cells need to survive.

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Biomarkers and MRI:

In patients with mild cognitive impairment refers to decline in their cognitive function, such as forgetfulness, but not so serious that there is dementia. In a subset of these patients, the disease is the cause of the complaints.

Patients with a reduction of the amyloid protein, and an increase of the tau protein in their cerebrospinal fluid and brain shrinkage in the MRI scan, had a greater chance of getting dementia due to Alzheimer's disease, than patients without this different biomarkers. Strikingly, the predictive value of the biomarkers was not the same for all patients, but for example, was lower for older patients.

Within the group of the patients with mild cognitive impairment due to Alzheimer's disease amyloid protein in the cerebrospinal fluid was found well suited to the Alzheimer's disease to establish at an early stage, but not to prevent further deterioration to predict. The concentration of the protein tau in cerebrospinal fluid and brain shrinkage on MRI showed indeed rapid deterioration of cognitive function.