Alzheimer’s disease (AD) is a condition whose main symptom is dementia. It is also the most frequent cause of Dementia in people over 60 years old. It is a progressive, neurodegenerative disease, that means symptoms usually develop slowly and get worse over time, becoming severe enough to interfere with daily tasks.
The most common early symptom of AD is difficulty remembering newly learned information, once the part of the brain responsible to process recent memory is first affected – a small area located in the temporal lobes called hippocampus. .As the disease advances other parts of the brain become affected. It leads to symptoms related to other high brain functions including disorientation, mood and behavior changes, confusion about events, disorientation in time and space. In early stages some people may be diagnosed with mild cognitive impairment (MCI). In the latest stages difficult to speak, swallow and walk can be present. This pattern of progression seems to be a protective measure , i.e. changes in less important functions occur before changes in essential brain functions ( it is less harmful to forget what you had for dinner the night before, than to lose the ability of walk or speak.)
Mild cognitive impairment (MCI) is a condition where the changes in cognition exceeds the normal, expected changes related to age. However, the cognitive changes are not so serious as to influence an individual’s social or professional life. It can be an early sign of Alzheimer’s. But, not everyone with MCI will develop Alzheimer’s disease. In other words, MCI is a very early stage of brain distress and should always be a “red flag” for the adoption of preventive measures and a healthy lifestyle.
MCI memory problems may include:
- Losing things often
- Forgetting to go to events or appointments
- Having more trouble coming up with words than other people the same age
Changes in the brain
Structural changes in the brain can be found in patients with AD and for long time ware thought to be specific of Alzheimer’s disease:
- Amyloid plaques (senile plaques) are deposits of a protein fragment called Beta-amyloid in the spaces between the nerve cells;
- Neurofibrillary tangles are twisted fibers of another protein called Tau protein built up inside brain cells.
Further studies have shown, however, that there are many normal patients with amyloid deposits, and also AD patients with very few amyloid deposits. Also, in the brain of elderly non-demented patients, the distribution of senile plaques is sometimes as extensive as that of dementia patients. This suggests that Aβ amyloid deposition has no direct relation with the onset of AD. Tau pathologies are also seen in other neurodegenerative dementing disorders. Such evidences have demonstrated that the classic pathological alteration described above occurs not only in AD and probably are not the primary cause of the disease, but a physiological response of brain tissue to aggressor factors. (See etiology for further information).
Anyways, it must be clear that AD begins affecting the brain many years before problems in memory, thinking and learning are noticeable. That means that AD is much more than only dementia, and that it starts silently and develops slowly.
That also means that we can prevent symptoms occurring, i.e. prevent dementia!
Das Gehirn und die Hauptverdächtigen bei Alzheimer (Quelle: Drs. Karner, Freiburg)
With the progression of the disease and the involvement of neurons function due to the presence of fibrillar entangled and senile plaques, atrophy (shrinking) of the affected brain regions occurs. Again the atrophy of the hippocampus is the first sign of the disease and can be observed on magnetic resonance imaging (MRI). Progressively, the entire cerebral cortex (the outermost layer of the brain formed by the gray matter) becomes atrophied and a widening of the ventricular system may be present.
History of Alzheimer’s dementia
In 1907, Aloysius “Alöis” Alzheimer carefully described the symptoms of a 51-year-old woman, Auguste Deter, who was under his care at the state asylum in Frankfurt. Alzheimer’s description of her symptoms is almost certainly the first neuropsychological characterization of the disease:
“Her memory is seriously impaired. If objects are shown to her, she names them correctly, but almost immediately afterwards she has forgotten everything. When reading a test, she skips from line to line or reads by spelling the words individually, or by making them meaningless through her pronunciation. In writing she repeats separate syllables many times, omits others and quickly breaks down completely. In speaking, she uses gap-fills and a few paraphrased expressions (“milk-pourer” instead of cup); sometimes it is obvious she cannot go on. Plainly, she does not understand certain questions. She does not remember the use of some objects.”
When Auguste Deter died, Alzheimer used the then-new silver staining histological technique to examine her brain microscopically. When he did so, he observed the senile plaques, neurofibrillary tangles, and amyloid angiopathy that were to become the hallmarks of the disease that now bears his name.
- Bondi MW, Edmonds EC, Salmon DP, Alzheimer’s Disease: Past, Present and Future. J I Neuropsychol Soc, Oct 2017, 23 (9-10): 818-831 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5830188/pdf/nihms937916.pdf
- Ropper AH, Samuels MA, Klein JP; Adams & Victor’s Principles of Neurology 10thedition, 2014. accessmedicine.mhmedical.com/book.aspx