While it has been commonly assumed that a deficit
in semantic memory underlies many of the clinical and cognitive
features of early Alzheimer's disease (AD), there
has been little agreement on what constitutes a proper
theoretical description of this impaired system. Currently,
most theories of this disorder fall into two categories:
those that posit degraded semantic representations, and
those that posit impaired retrieval operations with relatively
intact semantic representations. It is argued that each
position has both empirical and logical disadvantages that
have prevented the development of a consensus on how to
describe the pathology of semantic memory in AD. In this
paper we present the details and supportive evidence for
an alternative account of the semantic memory deficit of
AD: the Gain/Decay hypothesis. The core claim of the Gain/Decay
hypothesis is that a reduction in the time constant of
spreading activation in AD produces dynamic changes in
the availability of semantic representations that depend
on the time frame in which this information must be accessed.
The implications of this hypothesis for a range of experimental
and clinical phenomena are discussed, as are possible biological
correlates of the hypothesized alterations in the modulation
of activation. (JINS, 1999, 5, 641–658.)
The neural substrates of semantic memory deficits in early Alzheimer's disease: Clues from semantic priming effects and FDG-PET