Developing Epilepsy In Patients With Alzheimer’s Disease
AD is the most common reason for dementia that is predicted to influence 13. 8 million Americans by the middle of the century, driven mainly by increased percentage of the aged people1. Over 16 million unpaid American caregivers offered about 18. 4 billion hours of care to AD patients in 20171. The economic costs of AD are estimated to exceed $277 billion by the end of 2018. The increased risk of emotional disturbance and deleterious mental and physical health consequences of the family caregivers is another concern.
In Egypt, dementia is not identified as a health challenge due to the large proportion of young people. However, the current demographic conversion causes dementia to become an impending challenge. The statistical data on rates and costs of AD in Egypt are deficient. However, in one study, the prevalence of dementia in Wadi Ara was reported as 20. 46% for those aging 65 years. Pathologically, the main stamps of AD are the extracellular deposits of amyloid-beta protein (A?) forming neuritic plaques and the intracellular accumulation of abnormal hyperphosphorylated tau proteins forming neurofibrillary tangles (NFTs). Those pathological changes, directly or indirectly, result in loss of synaptic function, mitochondrial damage, microglial activation and nerve degeneration.
Patients with AD have an increased risk of developing seizures and epilepsy. Furthermore, electroencephalographic (EEG) interictal epileptiform discharges and electrographic seizures have been observed in transgenic mouse model of AD with over expressed mutated form of Amyloid-beta precursor protein (A?PP). Aluminum is a well identified neurotoxin that is involved in the development of AD9. It crosses the blood brain barrier via the high affinity transferrin receptors. The distinct brain regions show variable sensitivities to aluminium caused by the differences in the blood brain barrier mechanisms. Auminum preferentially accumulates in the hippocampus and the frontal cortex where it inhibits slow and fast axonal transports by damaging synaptic architecture. Moreover, aluminum increases expression of A?PP, and accelerates tau protein aggregation. It is a potent cholinotoxin that causes neuronal apoptosis and degeneration of cholinergic projections. These changes ultimately cause learning and memory deficits and therefore can be used as an animal model for AD.
LTG is a second generation antiepileptic agent that was approved by the Food and Drug Administration (FDA) for the mangement of partial and tonic-clonic seizure and for bipolar disorder. It acts as a blocker of several calcium, potassium, and sodium currents18. MEM is a neuroprotective drug that acts by uncompetitive blocking of the N-methyl-D-aspartate (NMDA) receptor, which in turn prevents excitotoxicity caused by excessive influx of calcium. AD and epilepsy may co-exist.
Treatment of epilepsy in elderly patients with AD is difficult and needs special attention due to numerous pharmacokinetic factors and the possibility of drug interactions.
