appunti del dott. Claudio Italiano
In 1901 a German psychiatrist, dr. Alois Alzheimer, he visited a young woman
who presented cognitive disturbance: he introduced to the lady some familiar
objects that she knew and had used several times, but the patient, invited
to describe what she had seen, did not remember their names, was not able to
connect the object to his memory, as she had lost her short-term memory. The
psychiatrist, in fact, spoke of "disorder of writing amnesia", but Mrs.
Auguste was actually the first patient diagnosed with Alzheimer's disease.
Alzheimer's is a disabling degenerative dementia, which has an early onset
and leads to death. In Italy it seems that 800 thousand people are affected
and around 30 million are patients in the world, usually women.
In recent studies, the genesis of the pathology seems to be related in a
metabolic disorder, as in the cadaver the accumulation of a substance,
beta-amyloid, is found in the brain neurons.
This substance derives, in turn, from the metabolism of a protein called APP
(the abbreviation means Amyloid Progenitor Protein) due to the activity of
an enzyme, alpha-secretase. In Alzheimer's patients, however, there is a
variant form of this enzyme, beta-secretase, which leads to the production
of an abnormal beta-amyloid, which accumulates, is not disposed of and
smears the membrane of neurons. This is the basis of an inflammatory process,
because the "scavenger" cells of the human body are activated, the
macrophages, which recall the neutrophils and part of an autoimmune
inflammatory process, against their structures with the release of cytokines
and interleukins and TNF, with destruction slow and gradual of residual
neurons
Other researchers talk about a further protein, called tau protein, which is abnormally phosphorylated, which accumulates in neuro-fibrillary clusters, affecting the cholinergic transmission neurons present in the hippocampus, responsible for this structure of the learning process and the memorization processes.
Also called "dementia of Alzheimer", it is precisely classified among
dementias because the patient is impoverished of his cognitive baggage,
unlike the oligophrenic patient, who is already born poor in knowledge. Here,
however, cognitive impairment is chronic and progressive.
The disease initially manifests itself as dementia characterized by amnesia,
that is, thought disorder and memory deficit, first only for sporadic events
in everyday life; then perspective memory is involved (for example,
forgetting commitments and appointments taken); then the episodic retrograde
memory (ie the subject does not remember the past) and the semantic memory
(the acquired knowledge) is affected.
Gradually, unfortunately, as the disease progresses, patients experience
other disorders:
- aphasia, ie incapacity to speak and
- apraxia, ie the ability to perform complex actions:
The complex actions are represented by:
Transitive gestures: concrete manipulation of objects in a simple
activity like
use a comb, a toothbrush, a match, a pin
in a complex activity such as lighting a candle with a box of matches,
packaging a package
Intransitive gestures: gestures that do not involve the use of objects (on
order and on imitation)
- symbolic: sign of the cross, military salute, say goodbye
- mentions: ironing, planting a nail, brushing your teeth
- imitated arbitraries: fingers crossed, to form an 8
Execution of arbitrary sequences: beat hand punch, palm, cut, fist, palm,
cut. Execution of contrasting gestures: strong blow - weak blow
The pathology can also affect:
- Graphic and constructive activities:
- spontaneous writing and dictation
- spontaneous and copied drawing of a triangle, of a daisy, of a house, of a
cube
- reproduction of geometric figures using toothpicks, use a Lego
- reproduction of graphic sequences (line, point, curve, point line, curve)
Although there is currently no effective cure, several therapeutic strategies have been proposed to try to manage Alzheimer's disease clinically; these strategies aim to pharmacologically modulate some of the underlying pathological mechanisms. Firstly, in Alzheimer's, the levels of acetic choline are decreased (cf. brain decay), whereby drugs are tried to restore their physiological levels of acetylcholine using cholinesterase inhibitors, to increase acetylcholine in the synaptic vial, inhibiting its destruction.
The drugs available are
physostigmine, galatamine, neostigmine. The donezepil, non-competitive inhibitor
of acetylcholinesterase, would seem more effective because, with a half-life of
about 70 hours, it allows only one administration per day (while Galantamine has
a half-life of 7 hours). An alternative approach to the disease could be the use
of non-steroidal anti-inflammatory drugs to control the inflammatory component
that destroys the neurons. The researchers also highlighted the protective
action of vitamin E (alpha-tocopherol), which seems to prevent lipid
peroxidation of neuronal membranes caused by the inflammatory process. We still
talk about excitatory drugs such as those that amplify the release of glutamic
and aspartic acid and increase intracellular free calcium.
It was therefore thought to use nootropic drugs ("thought stimulants"), such as
piracetam and aniracetam. Another, more recent, line of action involves the use
of drugs that act directly on the glutaminergic system such as memantine.
Non-pharmacological forms of treatment consist mainly of behavioral measures,
psychosocial support and cognitive training. Other care involves the use of the
film of life, a film of 30-60 minutes with images taken from family albums,
films shot in previous years, with a soundtrack obtained from music that
famously marked the various important periods of life; all this in order to
recall the memories and stimulate the brain, to slow down the disease.