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1.
Figure 1

Figure 1. From: Toward Fulfilling the Promise of Molecular Medicine in Fragile X Syndrome.

The promise of molecular medicine in psychiatric and neurodevelopmental disorders (see sidebar “The Promise of Molecular Medicine in Brain Disorders” for explanation).

Dilja D. Krueger, et al. Annu Rev Med. ;62:411-429.
2.
Figure 2

Figure 2. From: Toward Fulfilling the Promise of Molecular Medicine in Fragile X Syndrome.

Some milestones in defining the pathophysiology of fragile X syndrome (FXS). The current therapeutic efforts in FXS originate from the mixing of two independent lines of research: genetic research on FXS (left timeline, yellow) and basic neurobiology research on mGluR-dependent synaptic plasticity (right timeline, blue). The discovery that mGluR-LTD is exaggerated in Fmr1 knockout (KO) mice (17) led to the mGluR theory of FXS pathophysiology, culminating in the initiation of clinical trials to test the efficacy of mGluR5 antagonists in the treatment of FXS. Numbers in parentheses are reference citations. Fmr1, fragile X mental retardation 1; FMRP, fragile X mental retardation protein; mGluR, metabotropic glutamate receptor; LTD, long-term depression; MPEP, 2-methyl-6-(phenylethynyl)-pyridine.

Dilja D. Krueger, et al. Annu Rev Med. ;62:411-429.
3.
Figure 3

Figure 3. From: Toward Fulfilling the Promise of Molecular Medicine in Fragile X Syndrome.

Prospects for the treatment of a developmental brain disorder. (a) Divergence of brain maturation in normal development versus development in fragile X syndrome (FXS). This continuous divergence results in an accumulated deficit in individuals with FXS that increases with age. (b) Prospects for treatment of this accumulated deficit in FXS. Three scenarios are conceivable with respect to interventions that occur following symptom onset: (i ) The optimistic view assumes that pharmacological intervention after symptom onset results in near-complete reversal of associated phenotypes. (ii ) The pessimistic view is that after an initial window of opportunity, pharmacological approaches can no longer alter the course of the disorder. (iii ) The intermediate (but still hopeful) view suggests that pharmacological intervention can slow or prevent progression of symptoms, although it may not fully correct previously established impairments.

Dilja D. Krueger, et al. Annu Rev Med. ;62:411-429.

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