The most common cause of presenile dementia, Alzheimer’s disease is a chronic, progressive organic, mental disease due to atrophy of the frontal and occipital lobes. Onset is insidious with failure of memory for recent events and emotional changes, depression, anxiety, and unpredictable behaviours being the earliest symptoms. This stage is followed by progressive apathy, space perception disorders, a shuffling gait, slow and awkward movements, and jerky muscle contractions (myoclonus), and irreversible loss of speech and memory eventually leading to the late vegetative phase consisting of complete inability to think, move, or speak. The patient usually dies of pneumonia, heart attack, or stroke.
Alzheimer’s disease most commonly appears in mid-maturity, between the 50th and 60th year. Patients younger than 45 years are very rare. It is seen in over 32 percent of the population over 85 years and increases rapidly after that. While painfully aware of his or her situation, the patient may hide the disturbance for some years with some success. More frequent in women.
In post-mortem examination of victims of this condition Alzheimer noted a loss of cells in all cortical layers except the motor cortex and a degeneration of neurofibrils, the filaments found in and around nerve cells. Neurofibrillary degeneration and plaques are distinctive histopathological features of the cerebral cortex. In advanced cases of the disease autopsies reveal condensed clumps of these filaments between the nerve cells, known as Alzheimer's baskets.
Aetiology is unknown. It may be due to deposition of amyloid in the parenchyma of the brain, which is toxic to neurons and oligodendroglia. An alternative hypothesis is that deposition of amyloid is a secondary effect. The amyloid deposition is thought to be due to an abnormality in the amyloid precursor protein. The fact that many Down syndrome patients develop Alzheimer disease suggests a possibility of involvement of chromosome 21. Familial clustering and apparent generation-to-generation transmission are suggestive of autosomal dominant inheritance in some cases, but it is possible that there is a viral component in the aetiology. Some cases are familial (familial Alzheimer disease or FAD).
The term Alzheimer’s diseases was suggested by the German psychiatrist Emil Kraepelin (1856-1926).
Alzheimer’s disease is clinically very similar to Pick’s presenile dementia, which has onset about a decade earlier than Alzheimer’s. The two diseases are separate entities, however. Arnold Pick first described ”his” disease in 1892.
Alzheimer's pupil and co-worker, Gaetano Perusini, described four cases in 1910. One of them was Alzheimer's patient, Augusta D.
- A. Alzheimer:
Über eine eigenartigen schweren Krankheitsprozess der Hirnrinde.
Neurolisches Zentralblatt, Leipzig, 1906, 25: 1134. Ueber eine eigenartige Erkrankung der Hirnrinde.
Allgemeine Zeitschrift für Psychiatrie und psychisch-gerichtliche Medizin, Berlin, 1907, 64: 146-148. Über einen eigenartigen schweren Krankheitsprozess der Hirnrinde.
Zentralblatt für Nervenkrankheiten, 1907, 30: 177-178. Über eigenartige Krankheitsfälle des späteren Alters.
Zentralblatt für die gesamte Neurologie und Psychiatrie, 1911.
Alzheimer’s second patient, Johann F.
- M.B. Graeber et al:
Rediscovery of the case described by Alois Alzheimer in 1911: historical, histological and molecular genetic analysis.
Neurgenetics, 1997; 7.7a.
- G. Perusini:
Über klinisch und histologisch eigenartige psychische Erkrankungen des späteren Lebensalter.
Histologische und histopathologische Arbeiten über die Großhirnrinde mit besonderer Berücksichtigung der pathologischen Anatomie des Geisteskranken, Jena, 1910, 3: 297-352.