Synaptic slaughter in Alzheimer’s disease

doi:10.1016/j.neurobiolaging.2003.09.001

Neurobiology of Aging

Volume 24, Issue 8, December 2003, Pages 1023-1027

https://doi.org/10.1016/j.neurobiolaging.2003.09.001 Get rights and content

Abstract

Synaptic loss is currently established as the best neurobiological correlate of the cognitive deficits of Alzheimer’s disease (AD) [Ann. Neurol. 27 (1990) 457; Ann. Neurol. 30 (1991) 572]. We provide evidence that still living neurons lose synapses in AD, in addition to the synapse loss due to death of neurons. We also provide evidence indicating that in addition to loss of synapses, synaptic function is also affected in AD by decrements in transcript species related to synaptic vesicle trafficking.

Section snippets

Conclusion

The data showing reduced expression of messages related to synaptic vesicle trafficking in AD indicate new synapse-related markers in AD and suggest study of the molecular mechanisms responsible for these reductions. These indices of synaptic vesicle trafficking may not represent the most appropriate or only class of measures that may be informative with respect to synaptic function in AD. Other promising classes of synapse-related measures are being investigated including mitochondria

Acknowledgements

This work is supported by the Pioneer Award from the Alzheimer’s Association PIO-1999-1519. NIH Grant AG14441, and Anonymous Donor Grant to PDC.

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Synaptic slaughter in Alzheimer’s disease

Abstract

Section snippets

Conclusion

Acknowledgements

Neurobiol. Aging

Brain Res.

Prog. Brain Res.

Curr. Opin. Neurobiol.

Cell

Neurobiol. Aging

Lancet

Neurobiol. Dis.

The molecular machinery for secretion is conserved from yeast to neurons

Proc. Natl. Acad. Sci. U. S. A.

Deterioration threshold of synaptic morphology in aging and senile dementia of Alzheimer’s type

Anal. Quant. Cytol. Histol.