Individuals with Down Syndrome (DS) comprise about 10/4 of the moderately to severely mentally retarded population. As it is the leading genetic cause of mental retardation, much attention has been focused on both the physical and psychological attributes of DS. Specifically, precocious aging and its correlates in DS individuals have been scrutinized.

Neurological changes associated with aging in DS persons bear striking similarities to those changes seen in individuals afflicted with dementia of the Alzheimer type (DAT).

Brain cells become tangled and/or deformed, neurotransmitter production declines, and as a result, normal transmission, storage, and processing of information cannot take place. Behavioral degeneration similar to DAT also has been documented in roughly 30X of DS individuals over age 35 years.

The age at which subtle behavioral signs of DAT first appear in DS persons seems to vary from the third to fourth decade of life, however neuropathology has been discovered in DS persons as young as 15 years. A primary behavioral indicator of progressive neurological pathology is impairment or loss of visual short-term memory.

Individuals with Down syndrome

Short-term memory (STM) assessments for individuals with suspected dated older DS persons have been of digit span or delayed matching-to-scruple tasks which revealed only cursory information about processes of STM.

More rigorous evaluation of these processes would be valuable in outlining effects of presumed neuropathology to understand better implications for work, home, and educational management of DSindividuals.

Although much is known about normal as compared to retardedindividuals’ STM processing, it is yet unclear whether STM processes differ in DS persons as compared to other retarded persons of similar chronological and mental ages.

Such comparisons could prove valuable for two reasons:

(1) the brain pathology of DAT accompanies no form of mental retardation other than DS, therefore establishing a possibility of discrepancies in STM processing; and

(2) educational and management programs may need to structure learning environments differently for DS and non-DS persons if such neuropathology leads to dissimilar STM processing.

No evaluations of functional STM skills have been made in young and old DS individuals. Without comparisons within the DS population, it would be presumptuous to ascribe changes in STM abilities to age-associated Alzheimer like pathology.

Another issue of importance in characterizing the STM abilities of DS and non-DS retarded individuals is the effect of mnemonic strategy use in augmenting STM processes. Retarded individuals’ have been shown to profit from such strategies as rehearsal, imagery, and semantic cues.