Clinical Note

Alzheimer's Disease

Alzheimer's disease was first described by the German physician Alois Alzheimer in 1907. The disease is associated with a progressive decline in cognitive function (i.e., dementia), in general, and a specific impairment in the ability to retrieve old memories (retrograde amnesia) and form new memories (anterograde amnesia). Approximately 4 million individuals in the United States have Alzheimer's disease, and it has been estimated that the cost due to treatment and care of these individuals exceeds $100 billion per year. At the cellular level, the disease is associated with neuronal loss and the presence of neurofibrillary tangles and amyloid plaques. The amyloid plaques are extracellularly localized and consist primarily of ^-amyloid, a peptide derived from the transmembrane protein amyloid precursor protein. Neurofibrillary tangles consist of pairs of filaments wound around each other in a helical arrangement, thus giving rise to the term paired helical filaments (PHFs). The PHFs contain a hyperphosphorylated form of the microtubule-associated protein, tau. Plaques and tangles are found throughout the brain, but their greatest density is the hippocampus and cerebral cortex. This localization is consistent with the observation that most significant deficits associated with Alzheimer's disease are in episodic and semantic memory. There is no known cure for Alzheimer's disease. Alzheimer's disease is hypothesized to affect cholinergic neurons, thus attempts have been made to treat the disease by enhancing cholinergic neurotransmission. Two approved drugs are Aricept® and Cognex®. Both act by inhibiting acetylcholinesterase (see Chapter 6) and thus potentiating the effects of the acet-ylcholine released by undamaged cholinergic neurons. Note that a similar strategy is used to treat myasthenia gravis (see Chapter 6).

presented, the autoassociation network can complete the pattern; thus, any part of the stored pattern can be used as a cue to retrieve the complete pattern. For the example of Fig. 7, the input pattern was {101011}. This pattern led to an output pattern of {505055}. If the input pattern was degraded to {101000}, the output pattern would be {303022}. There is some change in the strength of firing, but the basic pattern is preserved. Autoassociation networks also exhibit a phenomenon known as graceful degradation. The network can still function even if some of the input connections or postsynaptic cells are lost. This property arises from the distributed representation of the memory within the circuit.

Note that the concept of distributed representation of memory crosses multiple levels of organization of memory systems. Multiple brain systems are involved in memory, and memory is distributed in different anatomical regions of the brain (see Fig. 1). Memory is distributed among synapses in a particular memory circuit (see Fig. 7), and memory at any one synapse is represented by multiple cellular changes (see Fig. 5).

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