Alzheimer's Disease

Synapses: the building blocks of memory

Alzheimer’s disease is the most common form of dementia. It is a progressive disease that is characterised by symptoms such as impairments in memory function, language, thought and problem-solving. In the earliest stages of the disease, memory loss is the most commonly reported symptom.

Loss of memory in Alzheimer’s disease is closely linked to loss of synapses, the connections between nerve cells.1

The brain communicates through a vast network of billions of nerve cells. These nerve cells or neurons connect with each other via junctions called ‘synapses’. Synapses allow communication between neurons and make it possible to create and recall memories. Throughout our lives, we continually lose and re-grow these important brain connections. In a healthy brain the amount of new synapses balances the loss of old ones, allowing for a sustained net number of synapses.2 The process of creating new synapses is called synaptogenesis and is the foundation of learning and memory.3,4 In the case of Alzheimer’s disease (compared with the normal aging process), the loss of synapses becomes accelerated. The loss of synapses is one of the key features of Alzheimer’s disease. Correlations have been observed between the number of synapses and cognition, with cognitive performance declining as the number of synapses decrease.5,6,7

Loss of synapses is the best pathological correlate of memory impairment in Alzheimer’s disease.7

Evidence is emerging that mechanisms of synaptogenesis are still present and activated in AD8,9,10. However, in AD the net balance of formation and breakdown shifts towards a net loss of synapses.11 This indicates a failure to maintain a stable net number of synapses in the face of the ongoing loss of neurons due to the pathology.

Nutrition is increasingly recognised as an important factor that influences risk of Alzheimer’s disease and its progression.12,13 Synapse formation depends on the availability of specific nutrients.14,15:  Consequently, insufficient availability of these nutrients may contribute to the net loss of synapses in Alzheimer’s disease.

View References

Selkoe DJ. Science, 2002;298(5594):789-91.
Trachtenberg JT, et al. Nature, 2002;420(6917):788-94.
Woollett K, et al. Curr Biol, 2011;21(24):2109-14. .
Maguire, EA, et al. PNAS, 2000; 97(8):4398-403.
DeKosky ST and Scheff SW. Ann Neurol, 1990;27(5):457-64.
Terry RD, et al. Ann Neurol, 1991;30(4):572-80.
Scheff SW, et al. Neurobiol Aging, 2006;27(10):1372-84.
Grady MS, et al. J Neurosurg, 1989;71(4):534-537.
Masliah E, et al. Neuron, 1991; 6(5):729-739.
Xu PT, et al. Mol Cell Neurosci, 2007;36(3):313-331.
Flood DG, et al. Prog Brain Res, 1990;83:435-443.
Gustafson DR, et al. J Alzheimers Dis, 2015;46(4):1111-27.
Vandewoude M, et al. Eur Geriatr Med, 2016;7(1):77-85.
Wurtman RJ, et al. Annu Rev Nutr 2009;29:59–87.
Van Wijk N, et al.J Alzheimers Dis 2014;38(3):459–79.