Longitudinal Neuropsychological Outcome in Taiwanese Alzheimer's Disease Patients Treated with Medication

Abstract

This longitudinal data shows the mean annual change of the MMSE, CASI, CDR, and CDR-SB in treated AD patients. The data may provide clinicians with information regarding to the cognitive decline rate in every year while their AD patients receive approved pharmacological therapy in real-world practice. Increasing age and severity of dementia when receiving therapy are the main factors that associated with faster deterioration.

Short-Term Response to Cholinesterase Inhibitors in Alzheimer’s Disease Delays Time to Nursing Home Placement

“…The result in this study-that initial response to ChEI, regardless of drug agent, delays NHP by 3 - 8 months-supports our previous observations that the responders exhibit slower disease progression and postponed endpoints in AD [ 15 , 16 ]. In agreement with other publications, no differences in effectiveness were demonstrated between the three types of ChEI [ 17 , 36 ]. We recently reported that improvement/no change after 6 months of therapy in cognitive, global, or functional capacities implied 0.5 years longer life-span on average [ 15 ].…”

“…Carriers of the APOE ε4 allele demonstrated a 45% increased risk of NHP in our basic ADL model, while in the other models, this characteristic showed a similar but nonsignificant trend. Some AD studies [ 17 , 34 , 35 ], but not all [ 36 ], found that presence of the ε4 allele could lead to a faster cognitive decline. Hence, like the aforementioned reports of predictors of response to ChEI, the significant predictors of longitudinal outcomes and endpoints in AD have been mixed and conflicting between studies.…”

Understanding and predicting the longitudinal course of dementia

“…Performance on neuropsychological assessments (NPA) also was an important disease characteristic evaluated as a predictor of dementia progression. In Alzheimer's dementia patients, free recall and category fluency at diagnosis were the most predictive of rapid cognitive [28], as was a low MMSE [11,29], high CDR [30] and worse Trail Making B [3]. In another study, patients with a non-memory impairments profile showed faster disease progression and higher risk of mortality than patients with most prominently memory impairment [31].…”

Clinical efficacy and safety of donepezil in the treatment of Alzheimer’s disease in Chinese patients

“…Similarly, no relationship was observed between APOE genotype and annual disease progression of mild to moderate AD patients receiving treatment with any AChEIs or memantine in their longitudinal study. 15 In another study, they reported a response rate (defined as CASI score change ≤0 from baseline) of 36.7% in 196 patients with mild to moderate AD after 1 year of treatment with donepezil (5 mg/d for 28 days followed by 10 mg/d thereafter), and further observed that white matter changes in the frontal area and basal ganglia were significantly associated with a reduced therapeutic response. 48 …”

“…14 Moreover, donepezil showed a similar effect as rivastigmine on ameliorating disease progression in a longitudinal observational study. 15 In a head-to-head study comparing galantamine and donepezil, both medications showed improvement in the Alzheimer’s Disease Assessment Scale-Cognitive Subscale (ADAS-cog) score after 16 weeks of treatment. 16 The total ADAS-cog, ADL, and Neuropsychiatric Inventory (NPI) scores were not significantly different between the two groups, although galantamine was superior for improving language function on ADAS-cog and had a higher response rate to treatment compared to donepezil.…”