Elsevier

The Lancet

Volume 355, Issue 9216, 13 May 2000, Pages 1696-1697
The Lancet

Research Letters
Longitudinal decline of the neuronal marker N-acetyl aspartate in Alzheimer's disease

https://doi.org/10.1016/S0140-6736(00)02246-7Get rights and content

Summary

In patients with Alzheimer's disease, but not in health controls, longitudinal magnetic resonance spectroscopy shows a striking decline in the neuronal marker, N-acetyl aspartate, despite little decline in underlying grey-matter volume.

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    NAA is involved in a variety of processes including protein synthesis, osmotic regulation and ATP metabolism (Homer, 1967; Birken and Oldendorf, 1989). Decreased NAA is thought to reflect neuronal or axonal damage and has been observed in bipolar disorder (Winsberg et al., 2000), multiple sclerosis (Caramanos et al., 2005) and Alzheimer’s disease (Adalsteinsson et al., 2000). A recent diffusion weighted MRS study found no change in NAA levels in their chosen ROI (the thalamus) following administration of LPS (De Marco et al., 2022), consistent with ex vivo studies that show no effect of LPS on NAA (Chang et al., 2005).

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    In contrast, decreased levels of NAA in several brain areas in MCI/AD have been long established (Gao and Barker, 2014), which is primarily thought of as an (unspecific) indicator of neuronal loss. However, reduced NAA seems to be more closely related to clinical disease progression than is cerebral atrophy (Adalsteinsson et al., 2000). Similarly, increased mI levels are a classic hallmark of MCI/AD pathophysiology, likely indicating glial activation, gliosis, and inflammation, and providing a link to protein-related AD neuropathology.

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