Gene/Protein Disease Symptom Drug Enzyme Compound
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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adult patients with Down syndrome show psychological symptoms and early senility. Improving their environment and dealing with their complaints and stress should first address their behavioral problems, such as self-injury, depression, aggression and outbursts. Pharmacological treatment may also be tried for behavioral disorders. Individuals with Down syndrome demonstrate neurotransmitter changes such as the loss of acetylcholine, norepinephrine, and serotonin (5-HT) with increasing age. Selective serotonin re-uptake inhibitor (SSRI) is effective for depression and panic disorders. We report here the effect of SSRI in two adult male patients with Down syndrome, 35 and 47 years of age. Self-injury in one case and aggression and outbursts in another improved after 1 week of fluvoxamine treatment, suggesting the effects of SSRI for behavioral disorders of adult Down syndrome.
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PMID:[Two cases of adult Down syndrome treated with selective serotonin re-uptake inhibitor for behavior disorders]. 1546 Oct 27

A previous report noted a 27% prevalence of autism in Joubert syndrome (JS), raising the question of overlapping etiologies. Family studies have shown that autism is characterized by family loading for a number of specific behavioral and psychiatric disorders and that the sib recurrence risk is around 4%. The purpose of this study is to determine whether children with Joubert and their families show behavioral or genetic characteristics similar to autism. Thirty-one volunteer Joubert families were identified. Parents completed a semi-structured family history interview and the Autism Behavioral Checklist. Rates of family loading for neuropsychiatric disorders in the JS families were compared to autism family history data and Down syndrome (DS) controls. The JS families had significantly lower rates of autism, alcoholism, cognitive, and language disorders than the autism families. Their rate of depression was lower, but not significantly different from that found in autism families. None of the JS children met the clinical cut-off for autism based on parental symptom report and the sib recurrence risk was 32% for the JS families compared to 4% for the autism and 0% for DS families. These data indicate that JS is a genetically distinct disorder from autism. Different genes with different inheritance patterns that affect neurodevelopment of the cerebellum could explain the clinical similarities previously reported in JS and autism.
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PMID:Joubert syndrome is not a cause of classical autism. 1563 74

This case study, of a woman with Down syndrome and dementia of the Alzheimer's type (DAT), follows the course of her decline over an 11-year period until death at age 57. Detailed neuropathological findings are also presented. This case illustrates features of premature aging that are typically associated with Down syndrome, and the progressive changes in memory and cognition that are usually associated with DAT. Although the subject's cardiovascular condition and thyroid disorder were treated, they may have contributed to the decline of her memory. This case shows the difficulty in diagnosing dementia in an individual with mental retardation who suffered comorbid episodes of depression and psychosis.
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PMID:Dementia of the Alzheimer's type and accelerated aging in Down syndrome. 1581 18

Due to the homology between human chromosome 21 and mouse chromosome 16, trisomy 16 mice are considered animal models of Down syndrome (DS). Abnormal hippocampal synaptic plasticity and behavior have been reported in the segmental trisomy 16 Ts65Dn mouse. In the Ts1Cje DS mouse model, which has a shorter triplicated chromosomal segment than Ts65Dn, more subtle hippocampal behavioral deficits have been reported. In this study, we investigated CA1 hippocampal synaptic plasticity, long-term potentiation (LTP) and depression (LTD) in the Ts1Cje mouse. Field excitatory postsynaptic potentials (fEPSPs) were recorded from the CA1 area of in vitro hippocampal slices from the Ts1Cje mouse and diploid controls, LTP was induced by a single tetanizing train pulse (1 s) at 100 Hz and LTD by a 900-pulse train at 1 Hz. We report for the first time that compared to diploid controls, the hippocampus from the Ts1Cje mouse had a smaller LTP and an increased LTD. The changes are less dramatic than had been reported previously for the Ts65Dn mouse. Furthermore, in the Ts1Cje mouse trains of pulses at both 20 Hz and 100 Hz produced a decrease in the evoked fEPSPs over the length of the train in comparison to diploid fEPSPs. These findings suggest that genes from Ts1Cje chromosome, including GIRK2 potassium channel, contribute to abnormal short- and long-term plasticity.
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PMID:Abnormal synaptic plasticity in the Ts1Cje segmental trisomy 16 mouse model of Down syndrome. 1599 87

Among the various phenotypes seen in Down syndrome (DS), mental retardation is the most common and most debilitating condition suffered by individuals with DS. The DYRK1A gene on human chromosome 21q22.2 encodes a subfamily of protein kinases that displays dual substrate specificities and is known to play a critical role in neurodevelopment. To study DS mental retardation, we have generated transgenic mice that contain only one copy of the complete human DYRK1A gene in a bacterial artificial chromosome. The transgenic mice showed significant impairment in hippocampal-dependent memory tasks in a Morris water maze. Interestingly, we observed shifts in both long-term potentiation and long-term depression, which suggests a role for DYRK1A in bidirectional synaptic plasticity. These mice represent the most clinically relevant DYRK1A mouse model to date and provide us a valuable tool for the in vivo study of mechanisms that underlie the learning and memory deficit in DS.
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PMID:DYRK1A BAC transgenic mice show altered synaptic plasticity with learning and memory defects. 1645 65

While dementia is often thought of as a problem unique to the elderly patient, nearly one in ten patients with dementia is younger than 65. The etiologies of dementia in this population are varied, including a genetically inherited form of Alzheimer's disease, as well as dementia related to other problems such as Parkinson's disease, Down syndrome, and cerebrovascular disease. Health care practitioners may have difficulty diagnosing early onset dementia because the diagnostic tools and the disease manifestation differ from those of the elderly patient. In addition, treatment of early-onset dementia can also pose unique challenges related to the speed of progression of the disease, depression, and behavioral disturbances, which often plague younger patients with dementia.
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PMID:Unique problems of dementia in the younger patient. 1654 45

The S100B is a Ca2+ binding proteins of EF-hand type and is produced primarily by astrocytes in the central nervous system. This protein has been implicated in the Ca2+-dependent regulation of a variety of intracellular functions such as protein phosphorylation, enzyme activities, cell proliferation and differentiation, dynamics of cytoskeleton constituents, structural organization of membranes, intracellular Ca2+ homeostasis, inflammation, and protection from oxidative cell damage. Recent studies suggest that released S100B exerts paracrine and autocrine effects on neurons and glia. On the other hand, elevations of S100B levels in blood or cerebrospinal fluid have been observed in patients with Alzheimer's disease, Down's syndrome, amyotrophic lateral sclerosis, multiple sclerosis, schizophrenia, depression, cerebral stroke and traumatic brain injury, and the levels have reached micromol/L-order at focal regions. It has been documented that the excessive S100B promotes the expression of inducible nitric oxide synthase or pro-inflammatory cytokines and exhibits detrimental effects on neurons. On studies using some animal models of the cerebral stroke or Alzheimer's disease, it is suggested that the excessive S100B produced by activated astrocytes precedes neurodegenerations. Authors discussed the relationship between neurological disorders and the S100B.
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PMID:[S100B: astrocyte specific protein]. 1663 91

Several lines of evidence suggest that loss of estrogen after menopause may play a role in the cognitive declines associated with Alzheimer's disease (AD). Women with Down syndrome (DS) experience early onset of both menopause and AD. This timing provides a model to examine the influence of endogenous estrogen deficiency on risk of AD. We hypothesized that low serum levels of bioavailable estradiol (E2) would be associated with increased risk of AD. One hundred and nineteen postmenopausal women with DS, 42-59 years of age, were ascertained through the New York State developmental disability service system and followed at 18-month intervals. Information from cognitive assessments, caregiver interviews, medical record review and neurological examination was used to establish the diagnosis of dementia. Women with DS who developed AD had lower levels of bioavailable E2, lower levels of total estradiol, higher levels of sex-hormone binding globulin, and lower levels of dehydroepiandrosterone sulfate at baseline than women who remained dementia free over the course of follow-up. Women who had low levels of bioavailable E2 at baseline were four times as likely to develop AD (HR=4.1, 95% CI: 1.2-13.9) and developed AD, on average, 3 years earlier, than those with high levels of bioavailable E2, after adjustment for age, level of mental retardation, ethnicity, body mass index, history of hypothyroidism or depression and the presence of the apolipoprotein varepsilon4 allele. Our findings support the hypothesis that reductions in estrogen following menopause can contribute to the cascade of pathological processes leading to AD.
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PMID:Bioavailable estradiol and age at onset of Alzheimer's disease in postmenopausal women with Down syndrome. 1692 67

The Interpersonal Model of Depression (IMD) based on the Theory of Human Relatedness (Hagerty, Lynch-Sauer, Patusky, & Bouwsema, 1993) is evaluated among adults with Down syndrome. One hundred subjects participated, with 32% having elevated depression scores and 40% stating they felt lonely. The relationship between depression, perceived social support, loneliness, and life satisfaction is statistically significant, F(6, 172) = 4.36, p < .001. Loneliness, social isolation, loss of sense of well-being, self-hate, and social withdrawal are important interpersonal manifestations and represent increasing levels of depression. Social and emotional loneliness are two dimensions of loneliness. The IMD provides a framework to assess depression in this population. Research on the efficacy of depression treatment based on the IMD is needed.
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PMID:Evaluating an Interpersonal Model of Depression among adults with Down syndrome. 1698 56

The mental health, adaptive behaviour and intellectual abilities of people with Down syndrome (n=129) were evaluated in a population-based survey of social and health care records. Females had better cognitive abilities and speech production compared with males. Males had more behavioural problems than females. Behaviour suggestive of attention deficit hyperactivity disorder was often seen in childhood. Depression was diagnosed mainly in adults with mild to moderate intellectual disability. Autistic behaviour was most common in individuals with profound intellectual disability. Elderly people often showed decline of adaptive behaviour associated with Alzheimer's disease. Case descriptions are presented to illustrate the multitude of mental health and behavioural issues seen from childhood to old age in this population.
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PMID:Mental health, behaviour and intellectual abilities of people with Down syndrome. 1704 8


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