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.1Selkoe D, Science. Published on 2002;298(5594):789-91.
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.2Trachtenberg JT, et al. Nature. Published on 2002;420(6917):788-94. The process of creating new synapses is called synaptogenesis and is the foundation of learning and memory.3Woollett K, et al. Curr Biol. Published on 2011;21(24):2109-14. ,4Maguire EA, et al. PNAS. Published on 2000; 97(8):4398-403. 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.5DeKosky ST and Scheff SW, Ann Neurol. Published on 1990;27(5):457-64 ,6Terry RD, et al. Ann Neurol. Published on 1991;30(4):572-80 ,7Scheff SW, et al. Neurobiol Aging. Published on 2006;27(10):1372-84.
Loss of synapses is the best pathological correlate of memory impairment in Alzheimer’s disease.8Scheff SW, et al. Neurobiol Aging. Published on 2006;27(10):1372-84.
Evidence is emerging that mechanisms of synaptogenesis are still present and activated in AD.9Scheff SW, et al. Neurobiol Aging. Published on 2006;27(10):1372-84. ,10Masliah E, et al. Neuron. Published on 1991; 6(5):729-739 ,11Xu PT, et al. Mol Cell Neurosci. Published on 2007;36(3):313-331 However, in AD the net balance of formation and breakdown shifts towards a net loss of synapses.12Flood DG, et al. Prog Brain Res. Published on 1990;83:435-443 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.13Gustafson DR, et al. J Alzheimers Dis. Published on 2015;46(4):1111-27 ,14Vandewoude M, et al. Eur Geriatr Med. Published on 2016;7(1):77-85 Synapse formation depends on the availability of specific nutrients.15Wurtman RJ, et al. Annu Rev Nutr. Published on 2009;29:59–87 : Consequently, insufficient availability of these nutrients may contribute to the net loss of synapses in Alzheimer’s disease.
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| 1 | Selkoe D, Science. Published on 2002;298(5594):789-91. |
|---|---|
| 2 | Trachtenberg JT, et al. Nature. Published on 2002;420(6917):788-94. |
| 3 | Woollett K, et al. Curr Biol. Published on 2011;21(24):2109-14. |
| 4 | Maguire EA, et al. PNAS. Published on 2000; 97(8):4398-403. |
| 5 | DeKosky ST and Scheff SW, Ann Neurol. Published on 1990;27(5):457-64 |
| 6 | Terry RD, et al. Ann Neurol. Published on 1991;30(4):572-80 |
| 7, 8, 9 | Scheff SW, et al. Neurobiol Aging. Published on 2006;27(10):1372-84. |
| 10 | Masliah E, et al. Neuron. Published on 1991; 6(5):729-739 |
| 11 | Xu PT, et al. Mol Cell Neurosci. Published on 2007;36(3):313-331 |
| 12 | Flood DG, et al. Prog Brain Res. Published on 1990;83:435-443 |
| 13 | Gustafson DR, et al. J Alzheimers Dis. Published on 2015;46(4):1111-27 |
| 14 | Vandewoude M, et al. Eur Geriatr Med. Published on 2016;7(1):77-85 |
| 15 | Wurtman RJ, et al. Annu Rev Nutr. Published on 2009;29:59–87 |
