Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuropsychologic test performance was examined in a normal control group and in three groups of Parkinson disease patients, with symptoms for 2 years or less, for 3 to 5 years, or for 6 to 15 years. On a test battery sampling a wide variety of cognitive and motor abilities, significant intergroup differences occurred primarily on tasks with a primary motor component, although mild intergroup cognitive impairment was also demonstrated. The results suggested that maximal deterioration occurred during the first 5 years of symptoms, with few significant additional changes after that.
 ...
PMID:The effect of symptom duration on cognitive and motor performance in parkinsonism. 57 44

Neuropeptide Y, one of the most abundant polypeptides within the nervous system, is co-stored with catecholamines, especially norepinephrine (NE), thus suggesting its possible involvement in pathologies characterized by a noradrenergic impairment. In Parkinson's disease (PD), as well as in multiple system atrophy (MSA), a central noradrenergic deficit has been demonstrated, and in the dementia of Alzheimer type (DAT) an impaired noradrenergic transmission has been postulated. In this study we determined CSF NE and MHPG levels in 29 PD, 15 MSA, 22 DAT patients and in 36 controls, while CSF NPY-immunoreactivity (NPY-ir) levels were measured in 10 PD, 7 MSA, 10 DAT patients and 20 controls. PD, MSA, and DAT patients showed a significant reduction in CSF NPY-ir and NE levels compared with controls, while CSF MHPG levels resulted in a reduction in only the MSA group. Furthermore, an inverse correlation between either NE or MHPG levels and the duration of the orthostatic hypotension was found in MSA patients while for DAT patients the MHPG levels were directly correlated to the severity of cognitive impairment, and inversely to the duration of illness.
 ...
PMID:Cerebrospinal fluid norepinephrine, 3-methoxy-4-hydroxyphenylglycol and neuropeptide Y levels in Parkinson's disease, multiple system atrophy and dementia of the Alzheimer type. 132 Aug 91

Lewy body dementia is common. It presents either with cognitive impairment and neuropsychiatric disturbance followed by parkinsonism or as dementia complicating established Parkinson's disease. It is unusual both in its pathological features and in its clinical manifestations. Although both overlap to some extent with those of Alzheimer's disease, Lewy body dementia is at least potentially recognizable during life. Some of its manifestations can be ameliorated by established methods, and it has pathological and neurochemical features which offer some hope for the development of useful palliative therapy. Major progress towards effective treatment is, however, likely to depend upon an improved understanding of the molecular mechanisms underlying its aetiology.
 ...
PMID:Lewy body dementia. 134 7

Somatostatin (somatotropin release-inhibiting factor, SRIF) was originally discovered (1) during the purification of growth hormone-releasing factor from rat hypothalamus and was subsequently isolated and characterized (2) in 1972 from ovine hypothalamus. Since its initial characterization, SRIF has been shown to fulfill criteria for a neurotransmitter and to directly modulate neuronal activity as well as acting as an inhibitory factor regulating endocrine and exocrine secretion. Alterations in cerebrospinal fluid (CSF) concentrations of SRIF have been reported in several diseases exhibiting prominent cognitive dysfunction, including Alzheimer's disease (AD), major depression, Huntington's chorea, multiple sclerosis, schizophrenia and Parkinson's disease, while evidence for regional brain tissue concentration deficits in SRIF are more specific for AD. This mini-review will focus on the studies reporting alterations in CSF and postmortem tissue concentrations of SRIF in AD and depression.
 ...
PMID:Somatostatin in Alzheimer's disease and depression. 135 21

A patient with progressive neurological deterioration characterized by cognitive impairment, myoclonus, Parkinson's syndrome, an abnormal electroencephalogram and fasciculations was considered for brain biopsy for suspected Creutzfeldt-Jakob disease. Complete clinical recovery followed discontinuation of lithium and nortriptyline. Awareness of this unusual drug-induced Creutzfeldt-Jakob like syndrome can avoid costly, invasive and unnecessary investigative procedures.
 ...
PMID:Drug-induced Creutzfeldt-Jakob like syndrome. 139 Jun 20

Evaluation with the geriatric depression scale carried out in 30 patients with Parkinson's disease who did not present subjective complaint of loss of memory or impairment in superior mental function capable of interfering in daily routine showed a high frequency of depression of 50-70% depending on where the cut-off in the geriatric depression scale was located. Depression in these patients does not significantly relate with either cognitive impairment or the degree of motor incapacity. Neither were depression or anxiety in these patients related with demographic data such as the age of the patient, age at onset of the disease, sex, months of evolution, or education. In contrast, a positive correlation was found between depression and anxiety.
 ...
PMID:[Depression in Parkinson's disease and its relation to the cognitive and motor manifestations]. 141 86

Although cognitive impairment is commonly associated with Parkinson's disease, the relative importance of cortical and subcortical pathologic changes to the development of dementia is controversial. Characteristic abnormalities in cortical glucose metabolism have been reported previously in Alzheimer's disease, a disease in which cortical changes predominate. We measured cerebral glucose metabolism with positron emission tomography in 20 control subjects and in 14 patients with PD with mental status ranging from normal to severely demented to determine whether changes in cortical glucose metabolism occur in early PD and whether the degree and pattern of metabolic change relate to the severity of dementia. The patients were divided into demented and nondemented groups according to the results of neuropsychological assessment. Age-adjusted covariance analyses were performed, since the age distribution varied between groups. The nondemented patients with PD showed widespread cortical glucose hypometabolism without any selective temporoparietal defects. The pattern of glucose hypometabolism seen in the demented patients with PD resembled that described in patients with Alzheimer's disease; ie, there was a global decrease in glucose metabolism, with more severe abnormalities observed in the temporoparietal regions.
 ...
PMID:Cerebral glucose metabolism in Parkinson's disease with and without dementia. 144 6

Silver techniques for intraneuronal cytoskeleton abnormalities (neurofibrillary tangles and neuropil threads) and extracellular A4-amyloid deposits were used to examine lesions of the cerebral cortex in six cases of progressive supranuclear palsy (three were mentally unimpaired and three showed moderate degrees of dementia). Deposits of A4-amyloid protein occurred in small numbers or were absent. Neurofibrillary tangles and neuropil threads were present in all cases and were largely confined to the allocortex. A characteristic pattern of changes was found in the entorhinal cortex. The three mentally unimpaired individuals had mild cortical changes virtually confined to the transentorhinal region while all of the demented patients showed severe destruction of the superficial cellular layer in both the transentorhinal and entorhinal region. This pattern of allocortical destruction closely resembles that seen in clinically incipient Alzheimer's disease or in mentally impaired cases of Parkinson's disease. The entorhinal region receives dense input from isocortical association areas and projects via the perforant path to the hippocampal formation. The cells of origin of major portions of the perforant path are located within the superficial entorhinal cellular layer. Destruction of this layer partially or totally disconnects the hippocampus from the isocortex. The specific pattern of entorhinal destruction is considered to contribute to cognitive impairment and personality changes, frequently seen in patients with progressive supranuclear palsy.
 ...
PMID:Allocortical neurofibrillary changes in progressive supranuclear palsy. 146 62

Two groups of patients with idiopathic Parkinson's disease underwent quantified electroencephalography (EEGq) using fast Fourier transfer to assess the effects of treatment with citicholine. Evidence of cortical cognitive impairment was seen in one group but not in the other. Certain parameters were established which enabled the two groups to be distinguished by examining specific EEGq indices. Specifically, differences were found in the overall potentials of the delta and alpha bands, in the alpha/theta index, in posterior activity, in the anteriorization index of the delta and alpha rhythms, and in the spatialization index of the alpha rhythm. The implications of these differences in the potential involvement of the frontal lobes in subcortical dementia in Parkinson's disease are discussed.
 ...
PMID:Effects of citicholine in subcortical dementia associated with Parkinson's disease assessed by quantified electroencephalography. 146 90

The cognitive performance of a group of 82 newly diagnosed patients with Parkinson's disease who had never been treated was reassessed approximately 4 mths after randomization to one of three monotherapies (levodopa, bromocriptine or anticholinergic drugs). Dopaminergic and anticholinergic treatments both led to improvement in motor control but their effects upon cognitive performance dissociated. Anticholinergic drugs produced impairment in processes underlying the immediate registration of information whilst dopaminergic therapy produced improvement on a task dependent on working memory and cognitive sequencing. Other cognitive measures showed no change on treatment. The deficits that were affected by cholinergic and dopaminergic modulation are those that were most compromised in the early, untreated state in Parkinson's disease. The data support the notion that cognitive impairment in Parkinson's disease is multifactorial in origin: short-term memory processes are served by both dopaminergic and cholinergic subcortico-frontal systems but much of the cognitive impairment of Parkinson's disease is independent of this subcortical neurochemical pathology and may be due to early neuronal dysfunction within the cerebral cortex.
 ...
PMID:Different effects of dopaminergic and anticholinergic therapies on cognitive and motor function in Parkinson's disease. A follow-up study of untreated patients. 148 57


1 2 3 4 5 6 7 8 9 10 Next >>