Fluoxetine in Alzheimer's disease with severe obsessive compulsive symptoms and a low density of serotonin transporter sites.

The treatment of behavioral disturbances is particularly challenging in patients suffering from dementia. In an 80-year-old female patient with probable AD and severe obsessive and compulsive symptoms, we demonstrated a significant reduction in the density of serotonin transporter sites using 1231-beta-CIT SPECT. Treatment with fluoxetine for 6 months resulted in significant symptom relief and an increasing density of serotonin transporter sites when compared to the beginning of treatment. Therefore, this report provides evidence that fluoxetine is a treatment option for patients with AD and severe obsessive-compulsive symptoms and highlights the importance of the serotoninergic system.

Pharmacological treatment strategies of residential primary care providers in dementia diseases--results of a representative survey in western Austria.

OBJECTIVE: The goal of this study was to investigate pharmacological treatment strategies used by residential primary care providers for patients with dementia. METHODS: A postal questionnaire survey was sent to all residential primary care providers, internists, neurologists and psychiatrists (n = 689) in the western region of Austria. RESULTS: The response rate (53 %) was similar in all four physician groups. Acetylcholinesterase inhibitors are considered to have a higher efficacy (p < 0.0005) compared to nootropic drugs. However, the vast majority of primary care providers (95 %) prescribe nootropic drugs. Two thirds (64 %) of the primary care providers prescribe acetylcholinesterase inhibitors. The dementia subtype influences the prescription frequency of acetylcholinesterase inhibitors, but not the specific choice of nootropic compound. Half of the primary care providers (52 %) combine antidementia drugs. Nearly two-thirds (62 %) of all primary care providers frequently prescribe antidepressants. Specific serotonin reuptake inhibitors are applied by the majority of primary care providers (96 %). About one-third (39 %) of primary care providers and internists (29 %) prescribe tricyclic antidepressants. Antipsychotics are applied frequently by around a quarter (29 %) of all physicians. More than half of primary care providers (62 %) and internists (58 %) treat patients with typical antipsychotics. Psychiatrists and neurologists are significantly more reluctant to prescribe tricyclic antidepressants and typical antipsychotics. CONCLUSIONS: Despite the lack of scientific evidence, residential primary care providers combine antidementia drugs very frequently. Therefore, controlled studies on combination therapies are urgently needed; in contrast to neurologists and psychiatrists, primary care providers and internists frequently prescribe tricyclic antidepressants and typical antipsychotics. The reasons for this should be clarified in further studies.

[Psychosocial therapy of patients with dementia]. / Die psychosoziale Therapie von Patienten mit Demenz.

The progressive cognitive and behavourial disturbancies in dementia diseases cause great emotional burden to patients, their families and caregivers. To relief this burden and to facilitate adequate coping strategies, psychosocial therapies intend to improve cognitive functions, self care abilities and emotional wellbeing of dementia patients. The therapeutic interventions address the patients, their caregivers and the adaption of the environment. Psychosocial therapies can be divided into cognitive training methods, behaviour orientated concepts, emotional orientated approaches and family interventions (1, 2, 12, 19). Most of these psychosocial therapies are only poor validated in randomized controlled trials. Nevertheless, they hold great promise to improve the quality of life and wellbeing of dementia patients and their caregivers. Thus they should be considered to be an integral part of a comprehensive therapeutic approach to dementia patients and their families.

[Alcohol-induced cognitive disorder: alcohol dementia]. / Alkoholinduzierte kognitive Störung: Alkoholdemenz.

Cognitive impairment is frequently observed in patients with alcohol misuse or alcohol addiction. Multiple cognitive functions are reduced in these patients. Frontal lobe functions, as planning, abstract thinking, set shifting or continuous performance are most frequently affected. Alcohol amnestic syndrome, alcohol dementia and the Wernicke-Korsakow-Syndrome constitute distinct entities. Alcohol dementia follows the diagnostic criteria of dementia with clear evidence for alcohol abuse or alcohol addiction. The diagnostic procedure of alcohol-induced cognitive impairment includes medical history, physical and neuropsychiatric examinations; laboratory examinations, neuropsychological assessment, brain imaging and electroencephalographic recordings. At the moment, there are no established treatment options for alcohol-induced cognitive impairment. Some evidence is provided that nootropics might be of benefit. Alcohol abstinence is a most important step. Psychosocial interventions are essential to support the patients in their daily activities.

Distribution of chromogranin B-like immunoreactivity in the human hippocampus and its changes in Alzheimer's disease.

Synapse loss is crucially involved in cognitive decline in Alzheimer's disease (AD). This study was performed to investigate the distribution and density of chromogranin B-like immunoreactivity in the hippocampus of control compared to AD brain. Chromogranin B is a large precursor molecule found in large dense-core vesicles. For immunocytochemistry we used an antiserum raised against a synthetic peptide (PE- 11) present in the chromogranin B molecule. Chromogranin B-like immunoreactivity was concentrated in the terminal field of mossy fibers, the inner molecular layer of the dentate gyrus and in layer II of the entorhinal cortex. In AD, chromogranin B was detected in neuritic plaques. The density of chromogranin B-like immunoreactivity was significantly reduced in the inner molecular layer of the dentate gyrus and in layers II, III and V of the entorhinal cortex in AD brains. The present study demonstrates that chromogranin B is a marker for human hippocampal pathways. It is particularly suitable for studying nerve fibers terminating at the inner molecular layer of the dentate gyrus. It is present in neuritic plaques, and its density is reduced in a layer-specific manner.

Synaptic loss reflected by secretoneurin-like immunoreactivity in the human hippocampus in Alzheimer's disease.

Secretoneurin is a recently described peptide derived by endoproteolytic processing from secretogranin II, previously named chromogranin C. In this study, we have investigated the distribution of secretoneurin-like immunoreactivity in the human hippocampus in controls and in Alzheimer's disease patients, and compared the staining pattern to that of calretinin. Secretoneurin-like immunoreactivity is present throughout the hippocampal formation. At the border of the dentate molecular layer and the granule cell layer, a band of dense secretoneurin immunostaining appeared. In this part, as in the area of the CA2 sector, the high density of secretoneurin-immunoreactivity coincided with calretinin-like immunoreactivity. The mossy fibre system displayed a moderate density of secretoneurin-immunoreactivity. In the entorhinal cortex, a particularly high density of secretoneurin-immunoreactivity was observed. The density of secretoneurin-like immunoreactivity was significantly reduced in the innermost part of the molecular layer and in the outer molecular layer of the dentate gyrus in Alzheimer's disease. For calretinin-like immunoreactivity, a less pronounced decrease was found in the innermost part of the molecular layer. About 40-60% of neuritic plaques were secretoneurin-immunopositive. This study shows that secretoneurin is distinctly distributed in the human hippocampus and that significant changes of secretoneurin-like immunoreactivity occur in Alzheimer's disease, reflecting synaptic loss.