Phosphatase and tensin homolog deleted on chromosome ten (PTEN) controls neuronal growth and synaptic function not only during embryonic and postnatal development but also throughout adult life.
Direct recruitment of PTEN to the postsynaptic membrane drives synaptic depression.
PTEN’s action at synapses is hijacked and exacerbated in response to amyloid β in Alzheimer’s disease (AD).
Preventing excessive recruitment of PTEN to synapses ameliorates cognitive function in AD mouse models.
Autistic disorders associated with PTEN loss of function are not exclusively the consequence of a defective neurodevelopmental program but may also reflect ongoing failures in synaptic depression because of insufficient PTEN activity at synapses.