1/23/2024 0 Comments Benzodiazepines temporary amnesia![]() 2 Behavioral studies to measure anterograde amnesia This review outlines the historical and current literature surrounding BZDs and anterograde amnesia, intending to inspire new research directions. Understanding these mechanisms could give greater insight into how these drugs might contribute to cognitive decline in aging and AD. The cellular and molecular mechanisms underlying BZD-induced anterograde amnesia and cognitive impairment are not fully understood. ![]() Acknowledging this observation, studying the relationship between BZD use in aging and Alzheimer’s disease (AD) is of great interest, as AD also results in atrophy of the medial temporal lobe. ![]() ![]() Interestingly, this amnesia is similar to the amnesia in patients with severe medial temporal damage ( Segura et al., 2021). More recently, healthy individuals showed impaired recollection of stories encoded immediately after diazepam administration ( Segura et al., 2021). This amnesia had a rapid onset of peak incidence 2–3 min after injection, with effects lasting around 1 h ( Dundee and Pandit, 1972). Anterograde amnesia, the inability to form new memories, was first observed in 1972 after intravenous injections of 10 mg of diazepam resulted in a reduction of recognition memory in 90% of women ( Dundee and Pandit, 1972). However, these drugs came with side effects, including impaired motor coordination, vertigo, mood swings, and anterograde amnesia ( Griffin et al., 2013).Īlthough anterograde amnesia is desirable during perioperative surgical periods and times of heightened anxiety, the long-lasting cognitive fog reported by patients needs to be addressed and better understood. Subsequently, other BZDs like diazepam were released in the early 1960s to improve the efficacy and potency of this new class of drugs ( Sternbach, 1979). The drug chlordiazepoxide, also known as Librium, was introduced in the 1960s and revolutionized the clinical use of sedatives ( Sternbach, 1979). In an effort to create a perfect tranquilizer, Sternbach and his associate Earl Reeder stumbled upon the compound that would soon become the first clinically available BZD. Understanding these mechanisms will allow for the development of alternative treatments and potentially allow BZDs to be used as a novel tool to study Alzheimer’s disease.īenzodiazepines (BZDs), a class of anxiolytic drugs, were invented in the mid-1950s by chemist Leo Sternbach. This review aims to inspire new research directions, as there is a gap in knowledge in understanding the cellular and molecular mechanisms behind BZD-induced amnesia. Additionally, the relationship between BZD use and cognitive decline related to Alzheimer’s disease is addressed, as there is a lack of consensus on whether these drugs are involved in inducing or accelerating pathological cognitive deficits. In this review we discuss, behavioral paradigms, sex differences and hormonal influences affecting BZD-induced amnesia, molecular manipulations, including the knockout of GABAa receptor subunits, and regional studies utilizing lesion and microinjection techniques targeted to the hippocampus and amygdala. However, these drugs come with the detrimental side effect of anterograde amnesia, or the inability to form new memories.
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