Acute Memory Loss Research Articles

Gamma radiation improves AD pathogenesis in APP/PS1 mouse model by potentiating insulin sensitivity

Alzheimer's disease (AD) is the largest unmet medical complication. The devastation caused by the disease can be assumed from the disease symptoms like speech impairment, loss of self-awareness, acute memory loss etc. The individuals suffering from AD completely depend on caregivers and have to bear the high cost of treatment which increases the socio-economic burden on the society. Recent studies have shown that radiation exposure can have therapeutic effects when given in suitable amount for a specific time period. Therefore, we investigated the role of gamma irradiation in AD pathogenesis. The effect of radiation on amelioration of disease progression was studied in AD transgenic mice model (APP/PS1). Our in-vivo studies using APP/PS1 mice demonstrated that a single dose of 4.0 Gy gamma irradiation improves AD associated behavioral impairment. Radiation exposure also increased the level of anti-oxidant enzymes and reduced the astrocyte activation in the brain of APP/PS1 mice. A significant reduction was observed in AD associated proteins (APP, pTau, BACE) and neurofibrillary tangle formations (NFTs). Exposure to a single dose of 4 Gy gamma radiation also increased glucose metabolic functionality in AD transgenic mouse model. The kinases involved in insulin signaling such as GSK, ERK and JNK were also found to be modulated. However, an increased level of GSK3β (ser 9) was observed, which could be responsible for downregulating ERK and JNK phosphorylation. This resulted in a decrease in neurofibrillary tangle formations and amyloid deposition. The reduced hyperphosphorylation of Tau can be attributed to the increased level of GSK3β (ser 9) downregulating ERK and JNK phosphorylation. Thus, a single dose of 4 Gy gamma irradiation was found to have therapeutic benefits in treating AD via potentiating insulin signaling in APP/PS1 transgenic mice.

A case for considering differences between organic and psychogenic amnesia

IntroductionMedical record, general examination, laboratory findings, neuropsychological interview and multidisciplinary consideration are essential to establish differencial diagnosis and correct approach in amnesic episodes.AimTo describe differences between organic and psychogenic anterograde amnesia.MethodsSingle case report and literature review.ResultsA 51-year-old man with only diagnosis of DM I, single, a good relationship with his family, without any personal or familiar psychiatric or neurological history, came to the hospital emergency department brought by his sisters referring disorientation, acute memory loss and mood changes, prevailing indifference to the situation for the last three days. After general exploration, including psychopatological examination and higher brain functions study, we arrived to the conclusion that the patient suffered from anterograde short-term severe amnesia as the only symptom, with evident conservation of autobiographic memory. The family referred as a possible stressor factor his mother's recent transfer to a different city, which had caused constant repeated questions about her location. Given the questionable presentation and trigger we shared the case with the neurologist, who ordered an array of tests to rule out any organic cause (LP, CT, MRI…), obtaining as a final result a diagnosis of limbic encephalitis, treated and effectively solved in two weeks with high-dose glucocorticoids.ConclusionCertain features of the symptoms exploration in amnesic episodes such as reiterative questioning about a specific topic, a non-modified autobiography or the absence of a clear traumatic precipitant factor, are essential for a correct approach and may lead the clinic to an organic evaluation.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Neuromyelitis Optica Spectrum Disorder Presented with Acute Memory Loss

Neuromyelitis Optica Spectrum Disorder Presented with Acute Memory Loss

Statin Therapy and Risk of Acute Memory Impairment

Reports on the association between statins and memory impairment are inconsistent. To assess whether statin users show acute decline in memory compared with nonusers and with users of nonstatin lipid-lowering drugs (LLDs). Using The Health Improvement Network database during January 13, 1987, through December 16, 2013, a retrospective cohort study compared 482,543 statin users with 2 control groups: 482,543 matched nonusers of any LLDs and all 26,484 users of nonstatin LLDs. A case-crossover study of 68,028 patients with incident acute memory loss evaluated exposure to statins during the period immediately before the outcome vs 3 earlier periods. Analysis was conducted from July 7, 2013, through January 15, 2015. When compared with matched nonusers of any LLDs (using odds ratio [95% CI]), a strong association was present between first exposure to statins and incident acute memory loss diagnosed within 30 days immediately following exposure (fully adjusted, 4.40; 3.01-6.41). This association was not reproduced in the comparison of statins vs nonstatin LLDs (fully adjusted, 1.03; 0.63-1.66) but was also present when comparing nonstatin LLDs with matched nonuser controls (adjusted, 3.60; 1.34-9.70). The case-crossover analysis showed little association. Both statin and nonstatin LLDs were strongly associated with acute memory loss in the first 30 days following exposure in users compared with nonusers but not when compared with each other. Thus, either all LLDs cause acute memory loss regardless of drug class or the association is the result of detection bias rather than a causal association.

Transient epileptic amnesia: Update on a slowly emerging epileptic syndrome

Transient epileptic amnesia (TEA) is a recently individualized, late-onset, pharmaco-sensitive form of mesial temporal lobe epilepsy with recurrent episodes of acute memory loss, but also interictal memory disturbances characterized by autobiographical and topographical memory impairment and a long-term consolidation deficit. In this article, we review the main clinical and electrophysiological characteristics of TEA, discuss its putative neuroanatomical substrate and mechanisms, common features and how it differs from related concepts, with the overall aim to defend the idea that TEA deserves to be recognized as a distinct epilepsy syndrome. While the pathophysiological basis remains largely unknown, emotional and/or dysimmune factors may have a potential influence. Most importantly, the concept of TEA is highly relevant to tertiary epilepsy and memory clinics, but also to routine neurology practice, leading to an adequate diagnosis and management of epilepsy-related, acute and long-standing memory deficits.

Reversible and Irreversible Stages in the Development of Amnesia after Disruption of the Reactivation of Associative Memory in Snails

Our previous studies on common snails have demonstrated that inhibition of NMDA glutamate receptors during reactivation of a skill consisting of refusal of a defined foodstuff leads to impairment of long-term memory. We report here our studies of the dynamics of the development of amnesia. Snails were trained to refuse a defined foodstuff and were injected 24 h later with the NMDA glutamate receptor antagonist MK-801, and were then presented with the conditioned food stimulus (a reminder). Testing on days 1 and 3 after exposure to MK-801 and the reminder showed gradual decreases in the number of refusals of the conditioned food stimulus. Repeat training of the animals to refuse the same foodstuff performed during these periods led to restoration of the skill seen after the initial training. The number of refusals by snails of the conditioned food stimulus 10 days after MK-801 and the reminder decreased to a minimal level. Repeat training at this time did not lead to the formation of a conditioned reflex to food. Thus, we have provided the first demonstration that impairment of the reactivation of long-term memory induces two stages in the development of amnesia. The first, reversible, stage, which lasted less than 10 days, was characterized by the potential for long-term memory to be restored by repeat training of the snails. The second, irreversible, stage developed 10 days after induction of amnesia and was characterized by disruption of the ability of long-term memory to be restored. These results may have practical value in terms of understanding the mechanisms of acute memory loss due to trauma and neurological diseases.

A puzzling case of transient global amnesia

A 47-year-old man presented to the emergency department in March, 2002, with acute memory loss. He declared no past medical history, and no vascular risk factors. He complained of moderate right lumbar pain and kept repeating the same questions. His blood pressure was 100/50 mm Hg, pulse; 60/min, oximetry; 100%. On examination, we heard a 3/6 systolic murmur at the aortic focus with cervical irradiation. The patient was disoriented in time, but not in place, and showed complete anterograde amnesia.