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. 2010 Mar 12;5:10. doi: 10.1186/1750-1326-5-10

Table 1.

Summary of potential targets of antidepressant drugs in relate to AD pathology

Antidepressants Neurogenesis Learning & memory NMDA Receptors
Fluoxetine
(SSRI)
Increase synaptic density in hippocampus[75] Does not interact with Aβ fibrils [159]. Protects hippocampal LTP [100]. Performance improvement in Morris water maze after chronic treatment [102]. Inhibit NMDA receptor directly [127].

Amitriptyline
(NSRI)
Does not increase synapse number but reduce decline in synaptic density [76]. Blocks age --induced deterioration of learning and memory [105].

Tiapentine
(atypical)
Prevents the reduction of dendrites length as a result of chronic stress [77]. Protects hippocampal LTP [99,100]. No effects on animal performance in Morris water maze[102] but improve animal performance is radial maze discrimination task [104].

TCA Reduce LTP in CA1 pyramidal cells [96,97]. Inhibit NMDA receptor directly [124,125].

Venlafaxine
(SNRI)
Performance improvement in Morris water maze after chronic treatment [101,103].

Imipramine
(NSRI)
Increase secreted APP, reduces intracellular APP in culture [165]. No effect on animal performance in Morris water maze [101] and even worsen spatial working memory in radial arm maze test [106]. Changes in binding to NMDAR [118,120]and expression of NMDAR in brain [116]

Citalopram
(SSRI)
Increase the levels of secreted APP in the medium of the treated neurons [165]. Adaptation of NMDAR complex [117]. Changes in expression of NMDAR [116].

Clomipramine (NSRI) Chronic administration changes the regulation of NMDA receptor control on the release of dopamine [119].

Milnacipran
(NSRI)
Antagonize NMDA receptor uncompetitively [126].

Paroxetine
(SSRI)
Reduces levels of Aβ and tau in Tg mice and cells [157,161-164]