Amnesia in healthy people via hippocampal inhibition: A new forgetting mechanism.

Structural damage to the hippocampus gives rise to a severe memory deficit for personal experiences known as organic amnesia. Remarkably, such structural damage may not be the only way of creating amnesia; windows of amnesia can also arise when people deliberately disengage from memory via a process known as retrieval suppression. In this review, we discuss how retrieval suppression induces systemic inhibition of the hippocampus, creating "amnesic shadow" intervals in people's memory for their personal experiences. When new memories are encoded or older memories are reactivated during this amnesic shadow, these memories are disrupted, and such disruption even arises when older memories are subliminally cued. Evidence suggests that the systemic inhibition of the hippocampus during retrieval suppression that gives rise to the amnesic shadow may be mediated by engagement of hippocampal GABAergic inhibitory interneurons. Similar amnesic shadow effects are observed during working memory tasks like the n-back, which also induce notable hippocampal downregulation. We discuss our recent proposal that cognitive operations that require the disengagement of memory retrieval, such as retrieval suppression, are capable of mnemonic process inhibition (the inhibition of mnemonic processes such as encoding, consolidation, and retrieval and not simply individual memories). We suggest that people engage mnemonic process inhibition whenever they shift attention from internal processes to demanding perceptual-motor tasks that may otherwise be disrupted by distraction from our inner world. This hitherto unstudied model of inhibition is a missing step in understanding what happens when attentional shifts occur between internally and externally oriented processes to facilitate goal-directed behaviour. This process constitutes an important novel mechanism underlying the forgetting of life events.

Prostaglandin analogs in ophthalmology.

Glaucoma is a major cause of irreversible blindness worldwide. Reducing intraocular pressure (IOP) is currently the only approach to prevent further optic nerve head damage. Pharmacotherapy is the mainstay of treatment for glaucoma patients. In recent years, a significant milestone in glaucoma treatment has been a transition to prostaglandin analogs (PGAs) as the first line of drugs. The rapid shift from traditional ß-blockers to PGAs is primarily due to their excellent efficacy, convenient once-a-day usage, better diurnal control of IOP, and systemic safety profiles. This review article aims to provide information regarding the various PGAs in practice and also the newer promising drugs.