Decreased activation along the dorsal visual pathway after a 3-month treatment with Galantamine in mild Alzheimer's disease
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Alzheimer's disease research has largely concentrated on the study of cognitive decline, but the associated behavioural and neuropsychiatric symptoms are of equal importance in the clinical profile of the disease. There is emerging evidence that regional differences in brain atrophy may align with variant disease presentations. The objective of this study was to identify the regions of decreased grey matter volume which were associated with specific neuropsychiatric behaviours in patients with mild Alzheimer's disease. Voxel-based morphometry was used to correlate T1-weighted MRI images obtained from 31 patients (19 male, 12 Female; mean MMSE 23.3, SD 2.8; mean age 77.1, SD 8.6) with mild Alzheimer's disease with specific neuropsychiatric symptoms and behaviours measured by the neuropsychiatric inventory. Delusions, agitation and apathy were significantly associated with specific regional tissue loss. Delusions were associated with decreased grey matter density in the left frontal lobe and in the right frontoparietal cortex. Agitation was associated with decreased grey matter values in the left insular cortex. Apathy was associated with grey matter density loss in the dorsal portion of the left anterior cingulate cortex, the head of the left caudate nucleus, the left frontal lobe, and bilaterally in the putamen. Neuropsychiatric symptoms of Alzheimer's disease may be associated with neurodegeneration of specific neural networks supporting personal memory, reality monitoring and neurobehavioural brain functions. The brain regions in which grey matter atrophy was independently correlated with delusions, agitation and apathy are similar to areas that have been associated with these symptoms in lesion, epilepsy, and schizophrenia, studies. The study of neurodegenerative disorders such as Alzheimer's disease using voxel-based morphometry and other imaging modalities may further an understanding of the neural structures that subserve social and emotional behaviour.
Apathy
Grey matter
Insular cortex
Voxel-based morphometry
Frontal lobe
Caudate nucleus
Cingulate cortex
Putamen
Cingulum (brain)
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This study would like to contribute to the understanding of the prognostic role of behavioral symptoms in mild cognitive impairment (MCI) for the progression to dementia due to Alzheimer's disease (AD). Data were generated through an ongoing prospective longitudinal study on behavioral symptoms in MCI and dementia. Behavioral assessment was performed by means of the MFS, Behave-AD, CMAI, CSDD and Geriatric Depression Scale 30-questions (GDS-30). Cox proportional hazard models were used to test the hypothesis that behavioral symptoms in MCI increase the risk for developing AD. The study population consisted of 183 MCI patients at baseline. At follow-up, 74 patients were stable and 109 patients progressed to AD. The presence of significant depressive symptoms in MCI as measured by the CSDD (HR: 2.06; 95% CI: 1.23 - 3.44; p=0.011) and the GDS-30 (HR: 1.77; 95% CI: 1.10 - 2.85; p=0.025) were associated with an increased the risk of progression to AD. The severity of depressive symptoms as measured by the GDS-30 was a predictor for progression too (HR: 1.06; 95% CI: 1.01 - 1.11; p=0.020). Furthermore, also the severity of agitated behavior, especially verbal agitation, and the presence of purposeless activity were associated risk factors for progression, whereas diurnal rhythm disturbances in our study was associated with a decreased risk of progression.
Geriatric Depression Scale
Depression
Longitudinal Study
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Neuropathology
Neurochemistry
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The pharmacological treatment of Alzheimer's disease is based on symptomatic therapy of cognitive decline and behavioral problems. Numerous therapies have been investigated for the treatment and prevention of Alzheimer's disease. We reviewed the current evidence-based medical research and guidelines of treatment for Alzheimer's disease. The use of cholinesterase inhibitors (ChEI) and N-methyl-D-aspartate (NMDA) inhibitors can bring about significant but modest therapeutic improvement. There is insufficient evidence to recommend vitamine E, estrogen, ginko biloba, or nonsteroidal anti-inflammatory drugs (NSAIDs) for the prevention or treatment of Alzheimer's disease. This article reviews the available data on current pharmacological treatments through evidence-based medicine.
Cholinesterase
Rivastigmine
Galantamine
Memantine
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It is hypothesized that treatment with memantine may delay the progression of driving impairment in patients with mild Alzheimer's disease. Driving is a hallmark of adulthood and independence. Slowing the progression of driving impairment in this population may extend the quality of life of those with Alzheimer's disease and ease the burden on their caregivers. Sixty otherwise healthy men and women ≥ 60 years with mild (MMSE ≥ 23) Alzheimer's disease were screened. 43 subjects met eligibility criteria and were randomized at a 1:1 ratio in a double-blind, 12 month trial of memantine 20 mg/day verses placebo. Stable doses of acetylcholinesterase inhibitors were permitted. Driving ability was measured by a standardized on-road driving test (DriveABLE). Cognitive performance was measured on a battery of driving-related neuropsychological assessments including measures of executive functioning, visuospatial ability, attention and orientation. The primary outcome measure was the number of subjects in each group able to pass the DriveABLE test at month 12 (endpoint). The secondary outcome measures were the change from baseline to endpoint on the cognitive assessments. Comparison of the treatment and placebo control groups at baseline indicates few significant differences in participant characteristics. There were no significant differences in age, gender, ethnicity or race. The groups did not differ statistically on mean MMSE, Fuld, Rey Figure or Trails A and B error rates. They did differ on Trails A and B time to complete. Placebo group participants required significantly more time to complete both Trails A and Trails B at baseline (p = .05 and .02 respectively). A greater percentage of treatment group participants reported having been involved in a prior crash (23% vs. 10%). This difference did not achieve statistical significance. Preliminary analysis suggests efficacy of memantine delaying progression of driving impairment. At 12 months, 100% of the treatment group either stayed the same or improved their driving ability, while only 75% of the placebo group did the same or better (p = .04).
Memantine
Neuropsychological test
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Vascular dementia
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Dementia, itself, neither implies a specific disease nor implies a specific underlying pathology. It refers to a change in cognitive function that is severe enough to compromise an individual's daily function. The Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) defines dementia as an acquired impairment of cognitive function that includes a decline in memory beyond what would be expected for age and at least one other cognitive function, such as attention, visuospatial skills or language, or a decline in executive functioning such as planning, organization, sequencing, or abstracting. The decline cannot only affect emotional abilities, but must also interfere with work or social activities. The deficits should not be accompanied by an impairment of arousal (delirium) or be accounted for by another psychiatric condition, such as depression or schizophrenia. Dementia can further be defined by a possible, probable, or definite etiologic diagnosis. A degenerative dementia implies disease progression over time.
Depression
Cognitive Decline
Affect
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