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 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Weight loss occurs frequently in patients with Alzheimer's disease (AD). This article will review why weight loss is so important in AD patients and what the ramifications are. This includes not only the negative effects of weight loss but possible benefits of weight gain. There is some evidence that weight loss manifests before AD. Structural, genetic, and neurochemical factors are discussed. There are possible risk factors and predictors which could herald weight loss in AD. Olfactory changes which occur in AD patients may make the food less appealing. Changes in food consumption may occur in AD leading to decreased energy intake. At the same time there is more evidence that increased energy expenditure is not the cause of weight loss in AD. Lastly we will go over possible treatment strategies. This includes environmental changes, food alterations, oral supplementations, and medications. A Medline literature search was conducted from 2000 to present using key search words of weight loss and Alzheimer's disease. Studies that were included were prospective designs, observational studies, review articles and their references.
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PMID:Weight loss in patients with Alzheimer's disease. 1828 91

Difficulty with lexical retrieval (naming, in common parlance) is a frequent complaint in many neurological diseases, as well as in more benign conditions such as aging and fatigue. Accordingly, neuropsychological tests of picture naming are widely used in the assessment of conditions such as Alzheimer's disease, head injury, epilepsy, stroke, and multiple sclerosis. However, nearly all of these tests were created and standardized on samples of Caucasian, monolingual English speakers. Using a thorough set of selection criteria, the current study identified a set of picture stimuli that should be valid for screening visual naming defects in bilingual Spanish/English speakers. A total of 51 pictures were identified, and data regarding important parameters of these stimuli (e.g., predominant response, types of responses) are provided. The results provide an important first step toward creating a valid neuropsychological screening test of English picture naming for Spanish/English bilingual speakers and have important clinical implications in light of the fact that this population is rapidly increasing in the United States.
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PMID:A screening test of English naming ability in bilingual Spanish/English speakers. 1860 56

Biological rhythms are periodic phenomena entrained to environmental changes by exogenous factors called synchronizers or entraining agents namely the light-dark cycle, the rest-activity cycle and the seasons, among others. In humans the major synchronizers are the light-dark and rest activity cycles. The endogenous component of a biological rhythm is dependent upon a number of clock genes. The main biological clock (oscillator or pacemaker) is the suprachiasmatic nucleus (SCN) of the anterior hypothalamus. The photoperiod (light-dark cycle) perceived by the retina acts on the SCN genes. Peripheral clocks have also been described in a number of tissues e.g. retina, adrenals. In a number of occurrences the synchronizers are badly perceived (transmeridian flights, shiftwork, nightwork...) or are not at all perceived (blindness). This situation is named rhythm desynchronization, it is external when the desynchronization is strictly related to the environment or internal when it is related to a dysfunction of the clock like in e.g. aging, Alzheimer disease, seasonal affective disorders (SAD) or hormone-dependent cancers which results in fatigue, sleep and mood disorders... A number of drugs called resynchronizing agents or chronobiotics which act on the biological clock are able to resynchronize the clock and to improve the patients' condition. Bright light is used in the treatment of SAD, melatonin, the pineal hormone, is also of interest when administered at precise timings in the 24hours scale. Other drugs like B12 vitamin or psychotropic drugs have also been proposed as chronobiotics.
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PMID:[Dysfunctions of biological clocks and their treatments]. 1870 43

Cognitive impairment and seizures are common in our aging population. Anticonvulsant treatment is problematic due to sedation, cognitive slowing, and behavioral changes. Levetiracetam has favorable pharmacokinetics, good efficacy in elderly individuals, a favorable side effect profile, and lacks major drug interactions. We conducted a prospective, uncontrolled, phase 4, open label, 12-week study of levetiracetam to better profile its efficacy, safety, and impact on cognitive/behavioral status in 24 cognitively impaired, elderly individuals. In total, 69% were seizure free for the duration of the study; the remaining participants had satisfactory seizure control. Fatigue was the most common side effect (5 participants). Significant overall improvements were observed for the Folstein's Mini-Mental State Examination and the Alzheimer's Disease Assessment Scale-Cognitive. No significant changes were seen in behavioral or functional measures. Levetiracetam is an effective antiepileptic drug in elderly individuals with cognitive impairment. At 3 months, participants who remained on levetiracetam showed excellent cognitive tolerability.
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PMID:Levetiracetam: a practical option for seizure management in elderly patients with cognitive impairment. 1900 51

The present article examines several lines of converging evidence suggesting that the slow and insidious brain changes that accumulate over the lifespan, resulting in both natural cognitive aging and Alzheimer's disease (AD), represent a metabolism reduction program. A number of such adaptive programs are known to accompany aging and are thought to have decreased energy requirements for ancestral hunter-gatherers in their 30s, 40s and 50s. Foraging ability in modern hunter-gatherers declines rapidly, more than a decade before the average terminal age of 55 years. Given this, the human brain would have been a tremendous metabolic liability that must have been advantageously tempered by the early cellular and molecular changes of AD which begin to accumulate in all humans during early adulthood. Before the recent lengthening of life span, individuals in the ancestral environment died well before this metabolism reduction program resulted in clinical AD, thus there was never any selective pressure to keep adaptive changes from progressing to a maladaptive extent.Aging foragers may not have needed the same cognitive capacities as their younger counterparts because of the benefits of accumulated learning and life experience. It is known that during both childhood and adulthood metabolic rate in the brain decreases linearly with age. This trend is thought to reflect the fact that children have more to learn. AD "pathology" may be a natural continuation of this trend. It is characterized by decreasing cerebral metabolism, selective elimination of synapses and reliance on accumulating knowledge (especially implicit and procedural) over raw brain power (working memory). Over decades of subsistence, the behaviors of aging foragers became routinized, their motor movements automated and their expertise ingrained to a point where they no longer necessitated the first-rate working memory they possessed when younger and learning actively. Alzheimer changes selectively and precisely mediate an adaptation to this major life-history transition.AD symptomatology shares close similarities with deprivation syndromes in other animals including the starvation response. Both molecular and anatomical features of AD imitate brain changes that have been conceptualized as adaptive responses to low food availability in mammals and birds. Alzheimer's patients are known to express low overall metabolic rates and are genetically inclined to exhibit physiologically thrifty traits widely thought to allow mammals to subsist under conditions of nutritional scarcity. Additionally, AD is examined here in the contexts of anthropology, comparative neuroscience, evolutionary medicine, expertise, gerontology, neural Darwinism, neuroecology and the thrifty genotype.
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PMID:Alzheimer's disease and natural cognitive aging may represent adaptive metabolism reduction programs. 1925 May 50

The purpose of this study was to explore factors that influence the clinical safety and tolerability associated with galantamine administration in Thai Alzheimer's disease patients with or without cerebrovascular disease and vascular dementia. This was an analysis of previous study. Tolerability and safety profile were analyzed according to sex, age, body weight, Thai mental state examination (TMSE) score, Alzheimer's disease assessment scale-cognitive subscale (ADAS-cog) score, and Alzheimer's disease cooperative study/activities of daily living (ADCS/ADL) score. The most common adverse events were nausea, dizziness, and weight loss which more often occurred during the dose-escalation phase. Mean body weight lost at week 24 was 0.9 kg. Sex, age, body weight, and ADAS-cog score did not influence the incidence of any adverse events. Dizziness was more likely to occur in patients with low TMSE and high ADCS/ADL score (p = 0.02 and p = 0.050, respectively). Patients with TMSE score equal or higher than 23 more often experienced muscle cramps and fatigue than who had TMSE lower 23 (p < 0.05). However, flexible dose escalation of galantamine with a 4-week schedule was safe and well tolerated in Thai AD patients.
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PMID:Safety and tolerability of galantamine in possible Alzheimer's disease with or without cerebrovascular disease and vascular dementia in Thai patients. 1956 80

This study investigated the relationship between self-reported sleep factors (sleep duration, insomnia, use of sleeping medicine, probable sleep apnoea and feelings of fatigue and tiredness) with cognitive functioning in 5177 people aged 30 years or older from a cross-sectional representative sample of the adult population in Finland (The Finnish Health 2000 Survey). Previous studies have indicated a U-shaped association between increased health risks and sleep duration; we hypothesized a U-shaped association between sleep duration and cognitive functioning. Objective cognitive functioning was assessed with tasks derived from the Consortium to Establish a Registry for Alzheimer's Disease test battery (verbal fluency, encoding and retaining verbal material). Subjective cognitive functioning and sleep-related factors were assessed with questionnaires. Health status was assessed during a health interview. Depressive and alcohol use disorders were assessed with the Composite International Diagnostic Interview. Medication was recorded during the health examination. Short and long sleep duration, tiredness and fatigue were found to be associated with both objectively assessed and self-reported decreased cognitive functioning. The association was stronger between sleep factors and subjective cognitive function than with objective cognitive tests. These data suggest that self-reported habitual short and long sleep duration reflect both realization of homeostatic sleep need and symptom formation in the context of the individual's health status.
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PMID:Self-reported sleep duration and cognitive functioning in the general population. 1994 91

Alzheimer's disease (AD) is attributable to synapse dysfunction and loss, but the nature and progression of the presynaptic structural and functional changes in AD are essentially unknown. We expressed wild-type or arctic form of beta amyloid(1-42) (Abeta) in a small group of neurons in the adult fly and performed extensive time course analysis of the function and structure of both axon and presynaptic terminals at the identified single-neuron level. Abeta accumulated intracellularly and induced a range of age-dependent changes, including depletion of presynaptic mitochondria, slowdown of bi-directional transports of axonal mitochondria, decreased synaptic vesicles, increased large vacuoles, and elevated synaptic fatigue. These structural and functional synaptic changes correlated with age-dependent deficit in motor behavior. All these alterations were accelerated in flies expressing the arctic form of Abeta. The depletion of presynaptic mitochondria was the earliest detected phenotype and was not caused by the change in axonal transport of mitochondria. Moreover, axonal mitochondria exhibited a dramatic reduction in number but a significant increase in size in aged Abeta-expressing flies, indicating a global depletion of mitochondria in the neuron and an impairment of mitochondria fission. These results suggest that Abeta accumulation depletes presynaptic and axonal mitochondria, leading to other presynaptic deficits.
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PMID:Expression of beta-amyloid induced age-dependent presynaptic and axonal changes in Drosophila. 2010 79

To improve the understanding of experiences of people with mild Alzheimer's disease (AD) and their significant others, related to the physical activity of the afflicted persons and its perceived importance. A qualitative case study design was used. The study comprised two men with mild AD and their wives. Data were collected by qualitative interviews and participant observations. Data analysis followed a thematic guideline as described by Braun and Clarke ( 2006 ). Three central themes of experiences related to physical activity in AD were identified: 1) physical activity as health reinforcement; 2) barriers to physical activity; and 3) adaptation strategies. Important motivations for outdoor walks were enjoyable experiences of nature, body movement, and positive attitudes toward physical activity. Several factors were experienced as barriers to physical activity (e.g., tiredness, difficulties in finding one's way, and "peculiar behavior"). Significant others made considerable adjustments in everyday life to enable their partners to retain a physically active lifestyle. The findings indicate that in persons with AD, physical activities such as outdoor walking can play an important part in everyday life by creating meaningful routines and improving experienced well-being and health.
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PMID:Physical activity and implications on well-being in mild Alzheimer's disease: A qualitative case study on two men with dementia and their spouses. 2039 57

Retigabine represents an antiepileptic drug possessing a completely different mechanism of action when compared to the existing classical and newer antiepileptic drugs. In the therapeutic range, retigabine enhances potassium currents, very likely via destabilization of a closed conformation or stabilization of the open conformation of the potassium Kv7.2-7.3 channels. There are also data indicating that this drug may be a GABA enhancer. Kainate-induced status epilepticus in rats resulted in massive apoptosis in the pyriform cortex and hippocampal area - retigabine inhibited neurodegeneration only in the former brain structure. The metabolism of retigabine has nothing to do with cytochrome P450 enzymes and the drug undergoes glucuronidation and acetylation. Randomized, placebo-controlled multicenter studies have shown that retigabine produced a considerable improvement as an add-on drug in patients with partial drug-resistant epilepsy. The most prominent adverse effects due to retigabine combined with the existing antiepileptic treatment were dizziness, somnolence and fatigue. The preclinical data indicate that this antiepileptic drug may possibly be applied in patients with neuropathic pain and affective disorders. Initial clinical data suggest that retigabine may be also effective in Alzheimer's disease or stroke.
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PMID:Retigabine: the newer potential antiepileptic drug. 2050 76


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