and other risk factors, and often includes symptoms such as memory impairment and problems with language, decision-making, judgment, and personality. the primary neurological phenomena that lead to the above symptoms are often related to signaling at excitatory synapses, often due to excitotoxicity, and stem from the presence of amyloid plaques and neurofibrillary tangles, as well as neuronal cell death and synaptic pruning. the principle drug treatments on the market deal with antagonizing glutamate (nmda) receptors at neuronal synapses, and inhibiting the activity of acetylcholinesterase. this treatment aims to limit the apoptosis of cerebral neurons caused by various pathways related to excitotoxicity, free radicals, and energy rundown. a number of labs are currently focusing on the prevention of amyloid plaques and other ad symptoms, often via the use of experimental vaccines, although this area of research is yet in its infancy. histological brain sample of the substantia nigra in parkinson's disease, showing the presence of lewy bodies and other signs of neurodegeneration. parkinson's disease (pd) is a neurodegenerative disease resulting from the apoptosis of dopaminergic neurons in the central nervous system, especially the substantia nigra, as well as heightened response to the excitatory neurotransmitter, glutamate (i.e., excitotoxicity). while the most obvious symptoms are related to motor skills, prolonged progression of the disease can lead to cognitive and behavioral problems as well as dementia. although the mechanism of apoptosis in the brain is not entirely clear, speculation associates cell death with abnormal accumulation of ubiquitinated proteins in cell occlusions known as lewy bodies, as well as hyperstimulation of neuronal nmda receptors with excessive glutamate neurotransmitter via the aforementioned pathway. like alzheimer's, parkinson's disease lacks a cure. therefore, in addition to lifestyle changes and surgery, the goal of pharmaceutical drugs used in the treatment of pd patients is to control symptoms and limit, when possible, the progression of the disease. levodopa (l-dopa), the most widely used treatment of pd, is converted to dopamine in the body and helps to relieve the effect of decreased dopaminergic neurons in the central nervous system. other dopamine agonists have been administered to patients in an effort to mimic dopamine’s effect at excitatory synapses, binding its receptors and causing the desired postsynaptic response.