Alzheimer’s disease is a degenerative disorder of the cerebral cortex that produces a dementia in middle to late life. It is a pathologic entity in that its ultimate defining characteristics are in neuropathology.The brain in disease gradually atrophies, nerve cells disappearing from the cortex. The major brunt of the atrophic process appears to be in the frontal and occipital regions of the brain, but microscopic examinations will demonstrate pathologic changes throughout the cortex. Many of the neurons that remain show a peculiar alteration of their neurofibrils.
These become thick and twist into distinctive “neurofibrillary tangles.” Within the atrophic cortex there are many “senile plaques.”These are microscopic collections of granular argyrophilic particles which tend to form in a halo around an indefinite center containing sudanophilic fat or an amyloid like substance. Exactly what these plaques are is uncertain, but they appear^ to represent collections of degenerating brain substance.
The dementia that accompanies Alzheimer’s disease has few distinctive characteristics. All the symptoms and signs enumerated above for dementia eventually appear. Onset is insidious and progress slow. A disturbance in recent memory is usually the first symptom. Affective disturbances such as depression or anxiety and disorientation in time and place appear soon after. Often there is a considerable emotional unrest in these patients, with some 30 to 40 per cent suffering at some time from distressing false beliefs of a delusionary character. A sizable fraction of patients also has hallucinations during illness.
What Causes Alzheimer’s Disease In Human Brain
Focal neurologic signs are rare early in the course of the disease, but with progression of the illness, focal cortical symptoms of aphasia, apraxia, and agnosia can become prominent. Seizures, both focal and generalized, are common only in far- advanced instances. With these intellectual and emotional disturbances there is the development of a disorder of gait. This takes the form of difficulty in starting the rhythmical movements of walking. A synchronous activation of agonist and antagonist muscles results in a locking of the legs and a hesitant shuffle.
The progress of all these symptoms is much the same in all patients. It is slow, but usually within five to eight years of the onset of symptoms the patient reaches a terminal stage. Here there is a profound dementia and a decerebrate physical state with flexion contractures of all limbs. Death comes from an intercurrent infection or some other complication of the bedfast condition.The age of onset varies.
Because this disorder was first recognized among relatively young people, the term “presenile dementia” has been applied to Alzheimer’s disease. This implies a distinction in kind between this condition and “senile dementia” that appears when many other changes of aging are evident. But the cerebral pathology and the clinical course of patients who develop symptoms before or after age 65 are the same. Alzheimer’s disease, defined as it is by the cerebral pathology of atrophy with senile plaques and neurofibrillary tangles, is a disorder appearing with increasing frequency as people age.
Alzheimer’s disease is not an uncommon disorder, but it is more common in females than in males. Autopsy diagnoses vary from 1 to 10 per cent in mental hospitals, the particular figure depending on whether the observers make a distinction between Alzheimer’s disease and senile dementia.
The etiology of Alzheimer’s disease is unknown. Most examples occur sporadically, but a few patients have a family history of dementia. It is not even certain whether Alzheimer’s disease is a specific response to one noxious biologic process or whether it is a more general response of the brain to injurious processes. The latter possibility is suggested by the occasional appearance of Alzheimer pathology in such different situations as the punchdrunk syndrome of boxers, Down’s syndrome (trisomy 21), and postencephalitic parkinsonism.
The diagnosis of Alzheimer’s disease is made most often by exclusion. An individual who has a slowly progressive dementia without prominent neurologic signs and without any of the clinical and laboratory findings of the treatable conditions mentioned, as well as a pneumoencephalogram demonstrating a moderate dilation of the cerebral ventricles with some atrophy of cortex, is most likely to be suffering from Alzheimer’s disease. Only by cerebral biopsy can more conclusive evidence for diagnosis be found, and this cannot be recommended in the usual clinical situations.
