Alzheimer's disease

(Alois Alzheimer, 1864 - 1915, German neurologist), the most common cause of dementia in the developed world. It is a heterogeneous disorder to which both genetic and environmental factors contribute. Microscopically, Alzheimer's disease is characterized by neuronal loss, gliosis, neurofibrillary tangles, senile plaques, Hirano bodies, granulovacuolar degeneration of neurons and amyloid angiopathy. Although histopathology is required to confirm the diagnosis, neuroimaging techniques are an integral part of the examination and follow-up of patients with dementia. CT and MRI are widely used in the evaluation of these patients. The two modalities differ in many aspects: CT has a lower contrast resolution compared with MRI and is also faster and often more convenient for patients. In contrast, MRI gives a superior picture of the brain tissue and does not suffer from bone artefacts. The latter is of special importance in the study of Alzheimer's disease where structural changes are present close to the brain. The possibility of imaging the brain in any desired plane also makes MRI more suitable for studying structures of relevance in Alzheimer's disease such as the temporal lobes and the hippocampal formation.

CT and MRI have delineated structural changes in Alzheimer's disease, including cerebral atrophy associated with cortical sulci widening and ventricular enlargement, and deep white matter lesions with periventricular distributions.

The brain of patients with Alzheimer's dementia shows diffuse cerebral atrophy. The degree of atrophy increases in parallel with the progress of the clinical stage. These changes are attributed to neuronal loss. Disproportionate atrophy of the temporal lobes, particularly the hippocampal formations, is a gross pathological hallmark of Alzheimer's disease. Specifically, the loss of hippocampal functions may be the cause of the memory deficits. In patients with histopathologically confirmed Alzheimer's disease the size of the medial temporal lobe is almost half that in age-matched controls and the rate of atrophy is 10-fold greater. The degree of medial temporal lobe atrophy is related to the density of neurofibrillary tangles in the hippocampus. Evaluation of the hippocampal atrophy by MRI scans has been reported to be a sensitive and possible specific indicator of mild Alzheimer's disease, while the possibilities of using functional MRI are currently being explored.

Functional MRI is a relatively new technique and can provide a measure of haemodynamic changes through the blood oxygen level-dependent (BOLD) signal. In a preliminary report, Alzheimer's disease patients had qualitatively focal areas of hypoperfusion in the posterior temporoparietaloccipital regions. Parieto-occipital hypoperfusion correlated with dementia severity.

Some Alzheimer's disease patients show hyperintense sylvian and/or hippocampaluncal cortex on long TR sequences on MRI. This signal reflects an increase in water content due to many of the histological substrates of Alzheimer's disease. Others have observed subtle gyral hypointense bands on long TR/long TE sequences, particularly in parietal regions due to iron or other paramagnetic accumulation.

In addition to the relatively specific findings described, MR and CT investigations have found that nonspecific white matter lesions can occur in Alzheimer's disease patients but there is no definite correlation with dementia severity. Severe subcortical and periventricular white matter disease is more typical of multi-infarct dementia.

Other diseases besides multi-infarct dementia that can mimic Alzheimer's disease clinically include subdural haematoma, primary brain tumours and normal pressure hydrocephalus.

LS