PD-related Dementia Research Articles

Mealtime Experiences of Families With Dementia

Twenty-three family caregivers participated in interviews to provide their perspectives on mealtimes when caring for someone with dementia (probable Alzheimer's disease, n = 14; senile dementia, n = 2; mixed dementia, n = 2; frontal temporal lobe dementia, n = 3; and Parkinson-related dementia, n = 1). Qualitative analyses described eating conduct changes and strategies to make mealtimes manageable. They also identified that mealtimes provided a social connection for families, although simplification of meals was required. Additionally, pleasure from food consumed was important, although tension existed around providing nutritious meals. Sometimes, caregivers compromised or "gave in"; at other times they needed to "step in" to promote a successful meal. The many changes noted around meals signaled the changing status of their family member. This study provides important insight into the challenges and benefits of mealtimes for those living with dementia in the community.

3.101 Functional connectivity in Parkinson's disease related dementia: A MEG study

3.101 Functional connectivity in Parkinson's disease related dementia: A MEG study

Dementia with Lewy Bodies: Therapeutic Opportunities and Pitfalls

To review diagnoses and challenges of treating patients with dementia with Lewy bodies (DLB), commonly considered the second most common form of dementia. 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. Articles describing studies, case series, and case studies are included in this review. 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. 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.

Update on dementia with lewy bodies

Dementia with Lewy bodies (DLB) presents to a range of specialists and involves a number of management challenges. The nosologic status of the disorder is controversial, especially its clinical overlap with Parkinson's disease-related dementia and its pathologic distinction from Alzheimer's disease. This article considers some of the controversies surrounding DLB with reference to recent literature. Emphasis is given to clinical topics, including the clinical phenomenology, differential diagnosis, and the treatment of core features of the disease.

Environmental enrichment inhibits spontaneous apoptosis, prevents seizures and is neuroprotective.

The mammalian brain has a high degree of plasticity, with dentate granule cell neurogenesis and glial proliferation stimulated by an enriched environment combining both complex inanimate and social stimulation. Moreover, rodents exposed to an enriched environment both before and after a cerebral insult show improved cognitive performance. One of the most robust associations of environmental enrichment is improved learning and memory in the Morris water maze, a spatial task that mainly involves the hippocampus. Furthermore, clinical evidence showing an association between higher educational attainment and reduced risk of Alzheimer and Parkinson-related dementia indicates that a stimulating environment has positive effects on cerebral health that may provide some resilience to cerebral insults. Here we show that in addition to its effects on neurogenesis, an enriched environment reduces spontaneous apoptotic cell death in the rat hippocampus by 45%. Moreover, these environmental conditions protect against kainate-induced seizures and excitotoxic injury. The enriched environment induces expression of glial-derived neurotrophic factor and brain-derived neurotrophic factor and increases phosphorylation of the transcription factor cyclic-AMP response element binding protein, indicating that the influence of the environment on spontaneous apoptosis and cerebral resistance to insults may be mediated through transcription factor activation and induction of growth factor expression.