The objective was to evaluate the course and severity of dementia-related symptoms and their relationship to caregivers' subjective burden and depression over time. Forty-five patients with dementia and their caregivers were followed over a period of 2 years. Patients' cognition, function, and behavioral/psychological symptoms were assessed by the Mini Mental State Examination, Syndrome Kurz Test, Geriatric Depression Screening scale, Instrumental Activities of Daily Living Scale, Physical Self Maintenance Scale, Behavioral Abnormalities in Alzheimer's Disease Rating Scale, and Nurses Observation Scale for Geriatric Patients. Caregivers' depression and subjective burden were evaluated by the Geriatric Depression Screening scale or Beck Depression Inventory and the Caregiver Burden Interview. Global dementia severity, functional impairment, and behavioral disturbances increased significantly over the 2-year observation period. Caregivers' burden remained stable, and severe depression decreased over time. There were significant associations between burden and dementia-related symptoms. For deficits in activities of daily living as well as behavioral disturbances, these associations became stronger over time. It was concluded that stage of dementia, functional deficits, and behavioral disturbances are important factors when evaluating the relationship between patients' symptoms and caregivers' well-being.

The electrophysiological results confirm prior findings of olfactory dysfunction in patients with Alzheimer's disease and preclinical Alzheimer's disease. Investigations of larger study groups with detailed cognitive examination and postmortem diagnosis may resolve the intriguing possibility of early diagnosis and discrimination of Alzheimer's disease subtypes through chemosensory event-related potentials in addition to existing biomarkers.

The CDT in combination with the MMSE or SKT is an easily administered, non threatening and highly sensitive screening test for dementia in the setting of a memory clinic.

No abstract

IntroductionSeveral hypotheses have been proposed as molecular basis explaining the enhanced neurodegeneration occurring during normal aging and Alzheimer's disease (AD). One of the most compelling is the role of free radical-induced oxidative stress in these disorders [1,16,17,22,24,25]. Enhanced oxidative stress during aging and AD is not restricted to the brain but also present in peripheral cells like fibroblasts [11] or lymphocytes [6,22,23]. Several oxidative stress-related changes in lymphocytes have been observed related to aging as for example diminished concentrations of antioxidants like a-tocopherol, ascorbat and glutathione [15] or age-associated changes in mitochondrial function including a decrease of several complexes of the respiratory chain and increased levels of oxidized mitochondrial DNA [6,12].Some of these changes ave additionally elevated in peripheral cells from patients with Alzheimer's disease (AD) like decreased glutathione (GSH) content [3] increased levels superoxide dismutase (MnSOD) mRNA [5] or increased lipid peroxidation [4]. Some findings indicate increased oxidative damage in lymphocytes of Alzheimer's disease patients [18 ± 21]. Moreover, similar changes may be induced by AD specific mutations of APP and PS1 genes. Gibson et al. demonstrated that fibroblasts bearing the AD Presenilin-1 246 Ala®Glu mutation have altered means of hand-