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At least 919 records · Page 51Linked to original sources
PubMed2003

Erotomania variants in dementia.

Erotomania is a delusional syndrome in which an affected individual is convinced that another person loves him or her. Erotomania usually occurs in middle-aged female patients. Only 3 cases have been described in dementia so far. The authors report 2 cases, in Alzheimer's disease and vascular dementia, in which erotomania emerged in the early stage of the underlying disorder. In both cases, erotomania partially responded to antipsychotic treatment. Erotomania may be understood in evolutionary terms as a pathologic deviation of an evolved psychological mechanism relating to mate selection and may therefore account for the typical sex distribution of the syndrome in favor of women and the onset of the disorder, usually during the late reproductive phase. The association of erotomania with dementing disorders may tentatively be interpreted to suggest that such complex psychological mechanisms and behaviors as involved here in "organic" delusions may have distinct, "hard-wired" representations in the human brain.

Aged↗
PubMedDate not supplied

Why do many NMDA antagonists fail, while others are safe and effective at blocking excitotoxicity associated with dementia and acute injury?

Similar to drug development programs for stroke and traumatic brain injury, programs developed for Alzheimer's disease (AD) have not been very effective in treating dementia. Recently, researchers have explored modulating excitatory synaptic neurotransmission via the N-methyl-D-aspartate receptor (NMDAR) to treat AD. However, many investigators doubt that NMDA antagonists are safe and effective for treating persons with AD because they have failed in stroke and trauma programs. This article explores the role of NMDA-mediated excitotoxicity in AD, reviews how the NMDAR functions, highlights the side effects and alternate signaling pathways that are initiated from NMDAR activation, provides examples of NMDA antagonists that do not exhibit the typical side effects, and discusses why some NMDA antagonist compounds are effective and safe in limiting cascades of excitotoxicity in dementia or acute brain injury.

Animals↗
PubMed1997

Neuropsychiatric adverse effects of antiparkinsonian drugs. Characteristics, evaluation and treatment.

Parkinson's disease (PD) is a progressive neurological condition that causes considerable disability in the elderly. Drugs used to treat PD, such as levodopa, offer symptomatic relief but often have neuropsychiatric adverse effects, most prominently psychosis and delirium. Aged patients and those with dementia are particularly vulnerable to these adverse effects. Evaluating PD patients with drug-induced neuropsychiatric adverse effects is made difficult by their complex clinical presentations. The treatment of drug-induced psychosis and delirium begins with manipulating the antiparkinsonian drug regimen, but this frequently worsens motor function. Atypical antipsychotics such as clozapine have been successfully employed to treat the psychosis without worsening the motor disability. Patient intolerance of clozapine therapy has prompted open-label studies with newer agents such as risperidone, remoxipride, zotepine, mianserin and ondansetron.

Aging↗
PubMed2002

Defining the role of the caregiver in Alzheimer's disease treatment.

The day-to-day responsibility of caring for a person with dementia often exacts a toll upon the caregiver, which may be manifested psychologically, physically, socially and financially. The last decade has witnessed the advent of drug availability for the treatment of Alzheimer's disease, specifically the cholinesterase inhibitors. Caregivers are integral to the initiation, administration and monitoring of treatment. In particular, they provide substitute informed consent when patients are no longer competent to do so. While there is evidence that cholinesterase inhibitors may reduce caregiver burden and time spent assisting patients, there are also burdens associated with being the person responsible for administering medication. Caregivers are key to research into the use of medications for Alzheimer's disease. They have roles in recruitment and consent and monitoring response and adverse effects. Increasingly, caregivers themselves are recognised as legitimate targets for evaluating the efficacy of new pharmacological agents for Alzheimer's disease (as benefits have been demonstrated for them). Caregivers have responsibilities regarding the drug treatment of patients with Alzheimer's disease, and require information about the medications so that they can have realistic expectations. Doctors need to work in partnership with caregivers and patients when prescribing drugs for Alzheimer's disease.

Activities of Daily Living↗
PubMed2006

From tau to toxicity: emerging roles of NMDA receptor in Alzheimer's disease.

Glutamate toxicity through NMDA receptor channels has long been central to the understanding of acute neuronal injury. Recent studies implicate similar events in chronic neurodegenerative diseases. Here, we analyze some of the most intriguing evidence for NMDA receptor-mediated cellular dysfunction and propose a mechanism by which hyperactive NMDA receptors might lead to neurofibrillary degeneration in Alzheimer's disease.

Activation Analysis↗
PubMed2006

Dementia with lewy bodies: therapeutic opportunities and pitfalls.

OBJECTIVE: To review diagnoses and challenges of treating patients with dementia with Lewy bodies (DLB), commonly considered the second most common form of dementia. DATA SOURCES: MEDLINE, Web of Science, and International Pharmaceutical Abstracts databases were searched in January 2006 for clinical studies, case series, case studies, letters, and review articles on the treatment of DLB. Search terms included: aripiprazole, cholinesterase inhibitors, clozapine, dementia with Lewy bodies, donepezil, galantamine, Lewy body dementia, neuroleptics, olanzapine, quetiapine, risperidone, rivastigmine, tacrine, ziprasidone. Applicable articles in the English language were reviewed. The bibliographies of these articles provided additional references. STUDY SELECTION: Articles describing studies, case series, and case studies are included in this review. DATA SYNTHESIS: DLB is commonly considered the second most common form of dementia, although some experts believe vascular dementia to be the second most common form. DLB is often under-diagnosed and misdiagnosed as Alzheimer's disease or Parkinson's related dementia. The core features of dementia with Lewy bodies are cognitive decline plus at least one of the following: fluctuations in cognition, visual hallucinations, and parkinsonism. Other supportive features include: neuroleptic sensitivity, repeated falls, syncope, transient loss of consciousness, REM sleep disturbances, depression, delusions, and nonvisual hallucinations. CONCLUSION: Increased prudence with the use of neuroleptic agents is essential in DLBs because the use of these agents is associated with physical and cognitive decline and increased mortality. While neuroleptic sensitivity has been reported with the use of both typical and atypical antipsychotic medications, these medications are often necessary for the treatment of psychotic symptoms. Decreases in neuroleptic sensitivity can often be achieved by dose reductions, although neuroleptic discontinuation is sometimes necessary. Cholinesterase inhibitors may be especially useful in the treatment of DLB. Cholinergic deficits are associated with visual hallucinations, and cholinesterase inhibitors often result in resolution of hallucinations, improved cognition, and decreased behavioral disturbances.

Antiparkinson Agents↗
PubMed1999

The role of probenecid-sensitive organic acid transport in the pharmacokinetics of N-methyl-D-aspartate receptor antagonists acting at the glycine(B)-site: microdialysis and maximum electroshock seizures studies.

The purpose of the present study was to determine whether the probenecid-sensitive organic acid transporter is responsible for the short duration of action of a new group of N-methyl-D-aspartate receptor glycine(B)-site antagonists, MRZ 2/570, 2/571, and 2/576. A prolongation of their anticonvulsant activity from 60 to 180 to 240 min, was found in mice after pretreatment with probenecid (200 mg/kg i.p.). Microdialysis studies in rats showed that this is likely due to a change in central nervous system concentrations of these drugs because cotreatment with probenecid caused an increase in the brain extracellular fluid half-life (0.5- to 4-fold) and the brain area under the curve (1.8- to 3.6-fold). In serum the half-life of MRZ 2/576 (30 mg/kg) was also increased by coadministration of probenecid from 15.6 +/- 1.3 to 40.6 +/- 6.0 min. At steady state (MRZ 2/576, 20 mg/kg/h i.v.), brain extracellular fluid concentration was elevated 2.5-fold by concomitant administration of probenecid. These results clearly show that these glycine(B)-site antagonists are rapidly cleared from the systemic circulation and the central nervous system by the probenecid-sensitive organic acid transport system. Moreover, the present data show that MRZ 2/570, 2/571, and 2/576 reach the brain in concentrations (1.34-2.32 microM) above the range of their in vitro potencies at the glycine site of the N-methyl-D-aspartate receptor (0.1-1.0 microM).

Animals↗
PubMed1999

Both the neuronal and inducible isoforms contribute to upregulation of retinal nitric oxide synthase activity by brain-derived neurotrophic factor.

Although neurotrophins are best known for their trophic functions, growing evidence suggests that neurotrophins can also be neurotoxic, for instance by enhancing excitotoxic insults. We have shown recently that brain-derived neurotrophic factor (BDNF) limits its neuroprotective action on axotomized rat retinal ganglion cells (RGCs) by upregulating nitric oxide synthase (NOS) activity (Klöcker et al., 1998). The aim of the present study was to investigate this interaction of BDNF and NOS in the lesioned adult rat retina in more detail. We used NOS immunohistochemistry and NADPH-diaphorase (NADPH-d) reaction to characterize morphologically retinal NOS expression and activity. Using reverse transcription-PCR and Western blot analysis, we were able to identify the NOS isoforms being regulated. Six days after optic nerve lesion, we observed an increase in neuronal NOS (NOS-I) mRNA and protein expression in the inner retina. This did not lead to a marked increase in overall retinal NOS activity. Only RGC axons displayed strong de novo NADPH-d reactivity. In contrast, intraocular injection of BDNF resulted in a marked upregulation of NOS activity in NOS-I-immunoreactive structures, leaving the level of NOS-I expression unchanged. In addition, an induction of inducible NOS (NOS-II) was found after BDNF treatment. We identified microglial cells increasing in number and being activated by BDNF, which could serve as the cellular source of NOS-II. In summary, our data suggest that BDNF upregulates retinal NOS activity by both a post-translational regulation of NOS-I activity and an induction of NOS-II. These findings might be useful for developing pharmacological strategies to improve BDNF-mediated neuroprotection.

Animals↗
PubMed2001

Drugs for treatment of Alzheimer's disease.

Alzheimer's disease is already an international problem of enormous significance, with an estimated 500,000 sufferers in the UK alone. There are currently four licensed compounds available for the symptomatic treatment of mild to moderate Alzheimer's disease, yet there is still considerable debate over their effectiveness. A variety of anti-dementia agents affecting the various aspects of the disease are in development and the debate will continue over the potential rationing of such treatments in the future. Drugs developed from the cholinergic and glutamatergic hypotheses will be discussed, and a number of other potential treatments aimed at reducing the oxidative stress and inflammatory response associated with dementia will be reviewed. The arrival of these new treatments for Alzheimer's disease has focused attention on the management of dementia in general and has provided the catalyst for the widespread development of memory clinics to enable proper assessment of patients with dementing disorders, providing hope for both patients and carers.

Alzheimer Disease↗
PubMed2001

[Current strategies of pathogenetic therapy of Alzheimer's disease].

This is a review of the data available in the literature and the authors' own findings on pathogenetical rationale for the use and clinical study of current treatments for Alzheimer's disease (AD) (synonym: Alzheimer-type dementia). In the past decade many attempts have been made at targeting different links of the pathogenesis of a neurodegenerative process that underlie AD. Several areas of pathogenetical therapy for AD have been developed on the basis of experimental studies and pilot clinical tests. The most developed areas are as follows: various compensatory (replacement) treatments aimed at overcoming neurotransmitter deficit in different neuronal systems that are damaged in AD to a greater or lesser extent; neuroprotective therapy promoting increased viability (survival) of neurons and their plasticity, and vasoactive therapy. Rather new directions of AD pathogenetic therapy, such as antiinflammatory and hormonal therapy along with antiamyloid therapeutic strategies are still under study.

Aged↗
PubMed1975

The effects of apomorphine and 1,3-dimethyl-5-aminoadamantane (DMAA) on ponto-geniculo-occipital (PGO) waves in cats.

The effect of AP and DMAA on the activity of Ro4-1284-induced PGO waves in lateral geniculate body (CGL) of cats is bidirectional. Higher doses decrease, whereas lower doses increase the intensity of PGO waves. DMAA inhibitis PGO activity in a dose-dependent manner. SP antagonizes AP inhibiting activity but does not affect the action of DMAA. The present study deals with the effect of AP and DMAA, the compounds stimulating central dopamine receptors, on the function of serotonin neurons.

Amantadine↗