And Alzheimer's Disease
in hypothalmic nuclei: Their relationship to neuronal
activity and clinical symptoms.
By D.F. Swaab, P.J. Lucassen, J.A.P. van de Nes, R. Ravid and A. Salehi
Graduate School Neurosciences Amsterdam, Netherlands Institute for Brain Research, Meibergdreef 33, 1105 AZ Amsterdam, The Netherlands
The neuropathological hallmarks of Alzheimer's disease (AD), i.e. amorphous plaques, senile plaques (SPs), pretangles, neurofibrillary tangles (NFT) and cell death are not part of a pathogenetic cascade but are basically independent phenomena. Pretangles can occur in neurons from which the metabolic rate is not altered. However, in brain areas where classical AD changes, i.e. SPs and NFT are present such as the CA1 area of the hippocampus, the nucleus basalis of Meynert and the tuberomamillary nucleus, a decreased metabolic rate is found.
Decreased metabolic rate also seems to be an independent phenomenon in Alzheimer's disease. It is not induced by the presence of pretangles, NFT or SPs. Decreased metabolic rate is considered to be crucial and an early occurring hallmark of Alzheimer's disease. In theory, decreased metabolic rate may be reversible. It is, therefore, attractive to direct the development of therapeutic strategies towards restimulation of neuronal metabolic rate in order to improve cognition and other symptoms in Alzheimer's disease.
Index of Slides
Alz-50 staining of nucleus tuberalis lateralis. Pre-tangle pathology without amyloid.
Golgi staining of nucleus basalis of Meynert. Evidence of neuronal inactivity.
Graph: Loss of neuronal activity in Alzheimer patients.
Decreased activity in tuberomamillary nucleus in AD. [Text only]
Paraventricular nucleus and the supraoptic nucleus don't show AD changes. [Text only]
No relation between decreased Golgi and plaques. [Text only]
Loss of Trk receptors in AD patients. [Text only]
Light-induced plasticity of suprachiasmic nucleus in AD patients. [Text only]