Alzheimer’s disease is the most frequently encountered form of dementia. Alzheimer’s disease is not the only cause of memory loss. The manifestations of Alzheimer’s disease range from the earliest signs of impaired memory to severe cognitive loss. Plateaus may occur where cognitive impairment does not change for a year or two but progression will subsequently resume.
The initial complaint is usually memory impairment for newly acquired information. Memory for remote events is relatively unimpaired at the beginning of the illness. With progression of the disease, problems with language, abstract reasoning, and executive functioning can be present. Depression and insomnia may occur. Delusions and psychotic behavior increase with the progression of Alzheimer’s disease. Hallucinations may be either visual or auditory. The neurological examination is usually normal except for impaired cognitive functioning.
Criteria for the clinical diagnosis of Alzheimer’s disease include a history of progressive deterioration in cognitive ability in the absence of other known neurologic or medical problems.
Changes may be seen on MRI scanning. Generalized slow activity may be seen on electroencephalography. PET scan shows hypometabolism in the temporal and parietal areas of patients with moderate to severe symptoms. The E4 polymorphism of the apolipoprotein E gene has been associated with a higher risk of Alzheimer’s disease but does not provide sufficient sensitivity or specificity to be used for diagnosis and is not recommended.
Alzheimer’s disease is characterized by atrophy of the cerebral cortex. The most characteristic pathology are the argentophilic senile plaques and neurofibrillary tangles. Scientists are unclear whether they cause Alzheimer’s disease or are the result of it. Amyloid is deposited on meningeal and cerebral vessels and in the gray matter. These gray matter deposits are multifocal, coalescing into structures known as plaques. Plaques are distributed in the brain in a characteristic fashion. Neurofibrillary tangles are fibrillary intracytoplasmic structures within the neurons composed largely of the protein tau.
Biochemically, the most consistent change is a reduction in the activity of choline acetyltransferase, the biosynthetic enzyme for acetylcholine in the cerebral cortex and hippocampus. There is a selective loss of cholinergic neurons. The severity of cognitive loss is roughly proportional to the loss of choline acetyltransferase.
Anticholinesterases are currently approved for treatment of Alzheimer’s disease and are considered palliative treatments. Anticholinesterases decrease the hydrolysis of acetylcholine released from the presynaptic neuron into the synaptic cleft by inhibiting acetylcholinesterase resulting in stimulation of the cholinergic receptor in the postsynaptic neuron.
Namenda (memantine) is indicated for the treatment of Alzheimer’s dementia and may be added to anticholine treatments. Namenda is an orally active NMDA receptor antagonist.
Incidence increases with age.
- Difficulty remembering newly learned information
- Memory loss serious enough to interfere with daily life.
- Mood and behavior changes
- Confusion about events, time, and place
- Unfounded suspicions about family and others
- Progressive memory and behavior changes
- Difficulty speaking, walking, and swallowing
- Memantine: An NMDA receptor antagonist