Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some genes are expressed differently in earlier and later generations of most cell lines. Many diseases become clinically expressed only later in life, and show clustering of the age at onset in the affected siblings, which may be related to the changing expression with age of the genes involved. Because insulin and its receptor are extremely ancient and well preserved structures with almost universal mitogenic effects, insulin may serve a paradigm of this process. It is suggested that by stimulating cell proliferation, hyperinsulinemia speeds up the appearance of later generations of cells with different expression of the genes. Insulin resistance, accompanying any hyperinsulinemia and considered to be a pathogenetic factor of some common later-age diseases, involves only some biochemical, but not mitogenic effects of the hormone. In humans, high levels of insulin in blood are encountered both physiologically after meals and in many pathological conditions: insulin therapy inevitably causes peripheral hyperinsulinemia; in type 2 diabetes hyperinsulinemia precedes hyperglycemia by many years; hyperinsulinemia is an independent risk factor of atherosclerosis, of type 2 diabetes itself, of some forms of dementia and other diseases; obesity is an obligatory hyperinsulinemic condition. The opposite of hyperalimentation, i.e. calorie restriction (at least, in rodents) may exert its life-prolonging effects through decreasing insulinemia and therefore the rate of cell proliferation. Insulin is only one example, and different mitogens regulate proliferation of different cells. It is likely that growth factors in general accelerating the replication of cells, play a role in speeding up the appearance of later-age diseases involving these cells.
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PMID:Mitogenic factors accelerate later-age diseases: insulin as a paradigm. 966 95

Hoarding behavior has been reported in several mental disorders and is occasionally reported by the caregivers of dementia patients. Such behavior may have adverse effects on the patients and increase the burden of the caregivers. This study was conducted to investigate the prevalence of hoarding behavior in patients with dementia and identify the characteristics and psychiatric symptoms associated with it. The sample was 133 dementia patients admitted to a geropsychiatric ward. Of the 133 dementia patients, 30 (22.6%) showed hoarding. Hoarding was found in various types of dementia. Patients with hoarding had a higher prevalence of repetitive behaviors, hyperphagia, and pilfering. Results suggested that hoarding behavior is a common symptom in dementia patients and a complex phenomenon. Better understanding of the underlying pathogenesis may highlight specific pharmacological or behavioral methods for treatment of the behavior.
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PMID:Hoarding behavior in dementia. A preliminary report. 979 76

Exonic and intronic mutations in Tau cause familial neurodegenerative syndromes characterized by frontotemporal dementia and dysfunction of multiple cortical and subcortical circuits. Here we describe a G389R mutation in exon 13 of Tau. When 38 years old, the proband presented with progressive aphasia and memory disturbance, followed by apathy, indifference, and hyperphagia. Repeated magnetic resonance imaging showed the dramatic progression of cerebral atrophy. Positron emission tomography revealed marked glucose hypometabolism that was most severe in left frontal, temporal, and parietal cortical regions. Rigidity, pyramidal signs and profound dementia progressed until death at 43 years of age. A paternal uncle, who had died at 43 years of age, had presented with similar symptoms. The proband's brain showed numerous tau-immunoreactive Pick body-like inclusions in the neocortex and the fascia dentata of the hippocampus. In addition, large numbers of tau-positive filamentous inclusions were present in axons in the frontal, temporal, and parietal lobes. Immunoblot analysis of sarkosyl-insoluble tau showed 2 major bands of 60 and 64 kDa. Upon dephosphorylation, these bands resolved into 4 bands consisting of three- and four-repeat tau isoforms. Most isolated tau filaments were straight and resembled filaments found in Alzheimer disease and some frontotemporal dementias with tau mutations. A smaller number of twisted filaments was also observed. Biochemically, recombinant tau proteins with the G389R mutation showed a reduced ability to promote microtubule assembly, suggesting that this may be the primary effect of the mutation. Taken together, the present findings indicate that the G389R mutation in Tau can cause a dementing condition that closely resembles Pick's disease.
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PMID:Tau gene mutation G389R causes a tauopathy with abundant pick body-like inclusions and axonal deposits. 1060 46

We describe the clinical and pathologic phenotypes of the G389R mutation in exon 13 of the Tau gene. Progressive aphasia and memory disturbance are the initial signs and begin in the fourth or fifth decade of life, followed by apathy, indifference, hyperphagia, rigidity, pyramidal signs and dementia. Death occurs after two to five years. Magnetic resonance imaging and neuropathologic studies show frontal and temporal atrophy. Pick body-like and axonal filamentous inclusions found in the neocortex and subcortical white matter, respectively, are tau immunoreactive. Immunoblot analysis of sarkosyl-insoluble tau shows two major bands of 60 and 64 kDa that, upon dephosphorylation, resolve into four bands of three- and four-repeat isoforms. Isolated tau filaments are often straight and occasionally twisted. Recombinant mutant tau protein shows a reduced ability to promote microtubule assembly, suggesting that this may be the primary effect of the mutation. The present findings indicate that the G389R mutation in Tau can cause a dementia similar to that in Pick's disease.
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PMID:Progress in hereditary tauopathies: a mutation in the Tau gene (G389R) causes a Pick disease-like syndrome. 1119 77

We examined 18 patients with problematic behaviors in relation to their individual characteristics and their possible relationship to certain aspects of dementia namely cognitive impairment, stage of illness, language impediment and functional disability. They formed part of an earlier assessment of 94 patients with dementia-related problems. Ten had altered eating habits and eight (8.5%) of them had hyperphagia. One exhibited an incomplete form of Kluver-Bucy Syndrome. Two had pathological stealing and one scatolia (smearing of faeces). The remaining had bizzare behaviors such as screaming and head banging. The majority of the patients were in the moderate category in relation to the four domains tested. The study revealed that behavioral problems in the more severe dementia becomes less of a problem to the caregivers and others. These behaviors could dramatically affect the social and interpersonal relationships resulting in community, family and caregiver burden.
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PMID:Some problematic behaviors in Alzheimer's dementia. 1125 Dec 39

Amongst factors associated with the institutional placement of elderly people with dementia, there has been little study of those related to malnutrition. We followed a cohort of 318 individuals with Alzheimer's disease (AD). Patients, who were all living at home at the start of the study were recruited from the outpatient service of a hospital unit specialising in AD. After one year, 20% of the patients had moved into institutional care. Multivariate analysis showed that a Mini nutritional Assessment score (MNA) of less than 25.5 (median score of the sample) and overeating behavioural problems (p=0.006) were risk factors for institutional placement. Nutritional problems are reversible and patients with a low MNA score could benefit from a thorough geriatric assessment, in order to slow or prevent institutional placement.
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PMID:Nutritional risk factors for institutional placement in Alzheimer's disease after one year follow-up. 1142 92

We report a kindred with three cases of dementia. The proband presented with forgetfulness and personality changes at age 56, followed shortly thereafter by behavioral dyscontrol, hyperphagia, hypersexuality, delusions, illusions, disinhibition and double incontinence. Neuroimaging studies were consistent with frontotemporal dementia (FTD). In one allele, an arginine insertion at codon 352 in the presenilin 1 (PSEN1) gene was identified; no mutation was identified in the amyloid precursor protein or tau genes. We conclude that the clinical features of the Kluver-Bucy syndrome and FTD can be associated with PSEN1 mutations. Furthermore, presenilin analyses may be helpful to characterize kindreds with familial dementing illnesses regardless of the phenotype, particularly if no tau mutation is present.
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PMID:Familial frontotemporal dementia associated with a novel presenilin-1 mutation. 1205 27

We describe a 57-year-old man (MW) with frontal variant frontotemporal dementia (fv-FTD) who presented with a long history of drinking problem and marital disharmony followed by gradual changes in personality with disinhibition, stereotypic checking, overeating and a decline in self-care. Structural MRI imaging confirmed marked frontal atrophy involving particularly the ventromedial region. Performance on standard tests of frontal executive function was largely unremarkable and MW obtained a perfect score on the Mini-Mental State Examination (MMSE). In contrast, an experimental battery of tasks designed to evaluate theory of mind (ToM) revealed marked deficits. MW's challenging and disruptive behaviours, notably obsessive checking of car suspension by rocking, and wandering, responded to behavioural modification regimes adapted from the neurorehabilitation literature. In conclusion, deficits in ToM may underline the gross abnormalities in social conduct, which characterise fv-FTD; ToM appears to dissociate from frontal executive function; and behavioural modification approaches can be of benefit in this disorder.
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PMID:Measuring and modifying abnormal social cognition in frontal variant frontotemporal dementia. 1216 38

A 81-year-old man, who had been diagnosed in multiple cerebral infarction and Alzheimer's disease, was followed up in his local clinic since 1997. He had been bedridden before admission, but could eat. He was admitted with severe aspiration pneumonia in December 1999. Since severe dementia and dysphagia were noted after admission, he was examined to find out whether or not he could swallow while the treatment of his pneumonia was conducted at the same time. The water swallowing test indicated a risk of aspiration, thus, percutaneous endoscopic gastrostomy was performed on January 26, 2000 after the completion of the treatment for pneumonia. Although the patient's condition was complicated by aspiration pneumonia, enteral feeding through the gastric fistula gradually became successful, and he was discharged in June 2000. His family physician followed him up by visiting at home to examine and observe his general physical condition including consciousness, vital signs, skin and respiration, while taking measures in cooperation with the local health care visiting nurse. The patient, thereafter, was repeatedly admitted and discharged because of exacerbation and remission of symptoms, including coughing, sputum and fever, probably caused by aspiration pneumonia. When he was admitted in December 2001, which was his sixth admission, since there were troubles with the infusion tube and frequent gastroesophageal reflux, the gastric fistula management was judged to be a great burden on the patient. In January 2002, the gastrostomy tube was removed and the patients, whose alimentation was managed using intra-venous hyperalimentation (IVH), was discharged. Besides periodic visits by his family physician, a 24-hour house visit system was introduced to control his IVH and deal with his family members' anxiety. His general condition, thereafter, has not markedly changed. The patient has continuously received medical treatment for 14 months after being discharged and his condition is stable.
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PMID:[A case of serious aspiration pneumonia associated with multiple cerebral infarctions and Alzheimer's disease followed by hospital and home care service team]. 1468 57

A byproduct of the aging of the population has been a dramatic rise in patients with dementia. The aim of the present study is to clarify the use of aggressive and palliative treatments, artificial nutrition and sedation in long-term care hospitals in Japan. We assessed 123 deaths in people aged 65 and older who died in two long-term care hospitals in and around Nagoya from January 2001 to December 2002. All deceased were divided into two groups according to their diagnosis of dementia. Data on the particular characteristics of the deceased, diagnosis of dementia, aggressive treatments (including CPR, intubation, mechanical ventilation, the use of systemic antibiotics and blood transfusion), palliative treatments (including oxygen, narcotic and nonnarcotic pain medication) artificial nutrition (including hyperalimentation and tube feeding) and sedation during the last six months of their lives were collected from medical charts. The prevalence of aggressive and palliative interventions did not vary significantly with the diagnosis of dementia except for the use of vasopressors. Artificial nutrition was prevalent and few patients received sedatives in either group. Patients with and without dementia received similar treatments in the end-stage. A greater understanding of the course of dementia is needed to further discussions on the terminal care of people with dementia. A national consensus on how to treat end-stage demented patients is also needed.
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PMID:[Terminal care for elderly patients with dementia in two long-term care hospitals]. 1499 24


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