Cognitive decline in temporal lobe epilepsy due to unilateral hippocampal sclerosis

Marques, Carolina; Caboclo, Luís Otávio Sales Ferreira; Silva, Tatiana Indelicato da; Noffs, Maria Helena da Silva; Carrete, Henrique; Lin, Kátia; Lin, Jaime; Sakamoto, Américo Ceiki; Yacubian, Elza Márcia Targas

doi:10.1016/j.yebeh.2007.02.002

Cited by 75 publications

(52 citation statements)

References 33 publications

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“…Patients suffering from epilepsy exhibit hippocampal sclerosis that may be correlated with cognitive decline in this population (Breteler et al, 1995;Thompson and Duncan, 2005;Marques et al, 2007). Animal models of epilepsy and seizures have also shown memory deficits and hippocampal damage similar to those reported in human studies (Cavazos et al, 1994;Gayoso et al, 1994;Gilbert et al, 1996).…”

Section: Discussionmentioning

confidence: 65%

“…The development of late onset seizures or epilepsy is a common occurrence in AD patients (Hauser et al, 1986;Romanelli et al, 1990;Hesdorffer et al, 1996) and some studies have even suggested that individuals suffering from epilepsy may be at risk of developing AD (Breteler et al, 1995;Thompson and Duncan, 2005). Studies in both humans and animals have shown subtle cognitive deficits following seizures, particularly in tasks requiring hippocampal involvement (Cavazos et al, 1994;Gayoso et al, 1994;Breteler et al, 1995;Gilbert et al, 1996;Thompson and Duncan, 2005;Marques et al, 2007). Seizure induced and other forms of excitotoxicity (e.g., increases in reactive oxygen species) appear to be linked to neurodegenerative diseases (Reiter, 1995).…”

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confidence: 99%

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Revisiting the cholinergic hypothesis in the development of Alzheimer's disease

Craig

Hong

McDonald

2011

Neuroscience & Biobehavioral Reviews

399

263

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Alzheimer's disease (AD) is the most common form of dementia affecting the elderly population today; however, there is currently no accurate description of the etiology of this devastating disorder. No single factor theory has been demonstrated as being causative; however, an alternative theory suggests that the interaction of multiple risk factors is responsible for AD. In this thesis I present data suggesting a neuroprotective role for acetylcholine during aging. Using a rat model of cholinergic depletion of the medial septum, I explored the effects of four common risk factors for AD (stress, seizures, stroke and circadian dysfunction) targeted at the hippocampus and examined the effects on measures of hippocampal dependent (water maze) and hippocampal independent (fear conditioning) memory. Here, I propose a role for acetylcholinemediated compensatory mechanisms in the functional recovery observed following sub threshold insults similar to those commonly observed in the elderly. m First and foremost I would like to thank my supervisor, Dr. Robert McDonald. Thank you for your support and encouragement, and for allowing me the independence to pursue my own projects and to learn from my experiences. I would also like to thank Nhung Hong for doing the majority of the cholinergic depletion and stroke surgeries used in this thesis and for teaching me the techniques. I would like to give a huge thank you to Joelle Kopp who was an invaluable asset who assisted in histology and spent many hours on the microscope counting cholinergic neurons. I would also like to thank Dr. Christine Werk for patiently reading and re-reading early drafts of my papers and this thesis and Dr.Hugo Lehmann for all his help in running statistics and interpreting my data. In addition, many thanks go out to Courtney Lamb, Robert Court and Arthur Verhoef for helping me with histology and behavioural testing, to Keri Colwell for running the corticosterone assays, the Metz lab for kindly allowing me the use of their microscope and to Karen Dow-Cazel and the rest of the animal care staff for taking care of my rats and helping me set up the circadian experiements. The cholinergic hypothesis of Alzheimer's disease 6 Acknowledgements IVThe basal forebrain cholinergic system 8The role of the basal forebrain cholinergic system in learning and memory 10The current state of the cholinergic hypothesis of Alzhimer's disease 15Risk factors for Alzheimer's disease 16Multiple combinations of co-factors theory of Alzheimer's disease 22The role of the hippocampus in learning and memory 24Objective of the present thesis 25Chapter 2: A series of pilot studies to determine the threshold for behaviourally sub threshold stroke, seizures and stress 28Abstract 29Experiment la: The effect of a chronic variable stress schedule on performance of the water maze task 32 Materials and Methods 33Results 36Experiment lb: The effects of a variable restraint stress procedure on levels of blood borne CORT 39 Materials and Methods 39Results 40Discussion 41Experiment 2: T...

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Section: Discussionmentioning

confidence: 65%

mentioning

confidence: 99%

Revisiting the cholinergic hypothesis in the development of Alzheimer's disease

Craig

Hong

McDonald

2011

Neuroscience & Biobehavioral Reviews

399

263

View full text Add to dashboard Cite

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“…So far, the origin of cognitive deficits of TLE still remains unknown. Theoretically, many factors may affect cognitive ability, including seizures themselves (Marques et al 2007), interictal epileptiform discharges (Aldenkamp and Arends 2004), and the reorganization of the underlying neuronal circuitry (Morimoto et al 2004;Seth 2008;Brown 2013). Although antiepileptic drugs can relieve epileptic seizures, some studies have revealed that these drugs also have some adverse effects on cognition (Meador 2006).…”

Section: Introductionmentioning

confidence: 99%

Exposure to Mozart music reduces cognitive impairment in pilocarpine-induced status epilepticus rats

et al. 2015

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Patients with temporal lobe epilepsy (TLE) often display cognitive deficits. However, current epilepsy therapeutic interventions mainly aim at how to reduce the frequency and degree of epileptic seizures. Recovery of cognitive impairment is not attended enough, resulting in the lack of effective approaches in this respect. In the pilocarpine-induced temporal lobe epilepsy rat model, memory impairment has been classically reported. Here we evaluated spatial cognition changes at different epileptogenesis stages in rats of this model and explored the effects of long-term Mozart music exposure on the recovery of cognitive ability. Our results showed that pilocarpine rats suffered persisting cognitive impairment during epileptogenesis. Interestingly, we found that Mozart music exposure can significantly enhance cognitive ability in epileptic rats, and music intervention may be more effective for improving cognitive function during the early stages after Status epilepticus. These findings strongly suggest that Mozart music may help to promote the recovery of cognitive damage due to seizure activities, which provides a novel intervention strategy to diminish cognitive deficits in TLE patients.

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“…The origin of cognitive comorbidity remains widely unknown. Many contributing factors have been proposed (Cornaggia et al, 2006), including seizures themselves Majak and Pitkanen, 2004;Marques et al, 2007), the abnormal electrical activities that occur between seizures , antiepileptic drugs (Meador, 2006), and the reorganization of the underlying neuronal circuitry (Morimoto et al, 2004). Seizures and the interictal activity (IA) that consistently occurs between seizures could negatively impact upon cognitive function, via saturation of long-term synaptic plasticity and interference with memory consolidation (Lopes da Silva et al, 1986;Kotloski et al, 2002;Majak and Pitkanen, 2004;Holmes and Lenck-Santini, 2006;Meador, 2007;Butler and Zeman, 2008).…”

Section: Introductionmentioning

confidence: 99%

Early Deficits in Spatial Memory and Theta Rhythm in Experimental Temporal Lobe Epilepsy

Chauvière¹,

Rafrafi²,

et al. 2009

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Patients with temporal lobe epilepsy (TLE), the most common form of epilepsy in adults, often display cognitive deficits. The time course and underlying mechanisms of cognitive decline remain unknown during epileptogenesis (the process leading to epilepsy). Using the rat pilocarpine model of TLE, we performed a longitudinal study to assess spatial and nonspatial cognitive performance during epileptogenesis. In parallel, we monitored interictal-like activity (ILA) in the hippocampal CA1 region, as well as theta oscillations, a brain rhythm central to numerous cognitive processes. Here, we report that spatial memory was altered soon after pilocarpine-induced status epilepticus, i.e., already during the seizure-free, latent period. Spatial deficits correlated with a decrease in the power of theta oscillations but not with the frequency of ILA. Spatial deficits persisted when animals had spontaneous seizures (chronic stage) without further modification. In contrast, nonspatial memory performances remained unaffected throughout. We conclude that the reorganization of hippocampal circuitry that immediately follows the initial insult can affect theta oscillation mechanisms, in turn, resulting in deficits in hippocampusdependent memory tasks. These deficits may be dissociated from the process that leads to epilepsy itself but could instead constitute, as ILA, early markers in at-risk patients and/or provide beneficial therapeutic targets.

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Cognitive decline in temporal lobe epilepsy due to unilateral hippocampal sclerosis

Cited by 75 publications

References 33 publications

Revisiting the cholinergic hypothesis in the development of Alzheimer's disease

Revisiting the cholinergic hypothesis in the development of Alzheimer's disease

Exposure to Mozart music reduces cognitive impairment in pilocarpine-induced status epilepticus rats

Early Deficits in Spatial Memory and Theta Rhythm in Experimental Temporal Lobe Epilepsy

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