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Many studies have suggested an association between anesthesia administered to older adults and cognitive decline and development or progression of Alzheimer's disease (AD).
Others have found that visual, rather than verbal, memory measures were predictive of memory decline and development of AD [ 32, 33].
aureus enterotoxins (19) have been associated with higher risk of lung function decline and development of chronic obstructive pulmonary disease (COPD).
Rett syndrome, the primary disorder caused by mutations in the X-linked MECP2 gene, is characterized by a period of cognitive decline and development of hand stereotypies and seizures following an apparently normal early infancy.
In accord with our findings, increasing evidence suggests a role for non-verbal memory measures, including rate of learning, in differential diagnosis of older adults with memory dysfunction [ 29, 30], as well as prediction of decline and development of AD [ 31– 31].
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In CaNoPy participants describe adapting to functional decline and symptom development, assuming ever decreasing choice in lifestyle rather than seeking assessment and support between clinic visits.
Significant increase in side effects during intensive therapy was observed (elevations of liver enzymes, muscle aches, cognitive decline and the development of diabetes mellitus) [ 38, 80- 83].
Such epidemiologic evidence for the prevention of cognitive decline and the development of dementia has been demonstrated previously for both estrogen replacement therapy and non-steroidal anti-inflammatory use.
Further studies assessing megakaryocytes, autoimmune anti-platelet antibodies, and virological response during combination therapy are warranted to elucidate factors associated with rapid early platelet decline, and consequent development of severe thrombocytopenia.
It is also possible that early progressive renal decline and the development of AER abnormalities are two clinical phenotypes that reflect the disease process underlying diabetic nephropathy that eventually results in ESRD.
However, to determine if hippocampal loss in normal subjects is already an indication of incipient Alzheimer's disease or other pathologies affecting the hippocampus requires clinical follow-up of the subjects to determine their cognitive decline and ultimate development of Alzheimer's disease.
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