Research published in the American Journal of Psychiatry demonstrates that elderly patients who are cognitively intact and diagnosed with major depression may have low levels of amyloid beta 42 (Aß-42) in cerebral spinal fluid (CSF).
Aß-42 has been implicated in Alzheimer’s disease as the main component of plaques. According to the authors, amyloid beta peptides also induce a depressive state in rodents and disrupt major neurotransmitter systems linked to depression. The authors assessed whether major depression was associated with CSF levels of amyloid beta, tau protein, and F2-isoprostanes in elderly individuals with major depressive disorder and age-matched nondepressed comparison subjects.
Results revealed that amyloid beta 42 levels were significantly lower in the major depression group (n=28) relative to the comparison group (n=19), and amyloid beta 40 levels were lower but only approaching statistical significance. In contrast, isoprostane levels were higher in the major depression group. No differences were observed in total and phosphorylated tau proteins across conditions. Antidepressant use was not associated with differences in amyloid beta 42 levels.
The study concluded that reduction in CSF levels of amyloid beta 42 may be related to increased brain amyloid beta plaques or decreased soluble amyloid beta production in elderly individuals with major depression relative to nondepressed comparison subjects. The researchers point out that “these results may have implications for our understanding of the pathophysiology of major depression and for the development of treatment strategies.”