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

The relative incidence of the major types of dementia disorders and the agreement rates between clinical and pathological diagnosis were analysed in consecutive autopsy series of 675 demented subjects from 3 hospitals (mean age 79.5 years, SD 9.6). Clinical assessment followed the DSM-III and ICD-9-NA criteria and NINCDS/ADRDA criteria for probable Alzheimer disease (AD) (McKhann et al. 1984), histological criteria for the diagnosis of AD those of the NIH/AARP Work Group (Khachaturian 1985) using a 4-degree rating scale for plaques and tangles in neocortex and hippocampus (Morris et al. 1988), and the criteria by Tierney et al. (1988) for 'pure' AD. Vascular dementia (MID) and other disorders were diagnosed according to current pathologic criteria. Clinical diagnosis of AD/SDAT was made in 59.2%, of MID in 21.7%, of mixed AD + MID in 3.1%, and of Parkinson's disease (PD) and other disorders in 16%. At autopsy, 76.7% fulfilled histological criteria for AD/SDAT, but only 60% were 'pure' forms, while 8.2% had additional features of PD and 7.9% coexisting vascular lesions indicating mixed SDAT + MID. 15.7% were MID with no or very little AD pathology, 7.4% other CNS disorders. 0.3% of the brains showed no abnormality beyond age-related changes. AD/SDAT had its highest incidence in a psychiatric population, MID and PD + SDAT in general and geriatric hospital cohorts. The overall coincidence rates for clinical and pathological diagnosis of AD/SDAT were 85.2%, for MIX and MID 60.5-61.9%, but only 51% for PD-PD/AD. These data and the results of other recent studies emphasize the need for more appropriate clinical and pathological criteria in the diagnosis of the dementias.
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PMID:Clinicopathological analysis of dementia disorders in the elderly. 235 19

AD is by far the leading cause of dementia, accounting for about 75% of cases. Vascular dementia and Parkinson's disease, with or without concomitant AD, are responsible for much of the remainder of pathologically confirmed causes of dementia. The differential diagnosis of AD remains clinically based; even in the absence of a biologic marker for the disease, diagnostic accuracy can be high. Informant interviews can be helpful in detecting early dementia and in distinguishing the various stages and features of AD. Characterization of phenotypic variants of AD and refinement of diagnostic criteria for the non-AD dementias is needed to clarify the inter-relationships of these conditions and facilitate molecular genetic and other basic investigations of the etiopathogenesis of AD.
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PMID:Differential diagnosis of Alzheimer's disease. 803 98

The aetiology of the common dementias of old age remains incompletely understood. Here we describe some of the biological, neurophysiological and psychological changes associated with ageing of the human brain, in terms of those that occur throughout life and those that are characteristic of senescence. Age-dependent diseases, such as Alzheimer's disease (AD), idiopathic Parkinson's disease (IPD) and dementia with Lewy bodies (DLB), are considered from these viewpoints, and risk factors described. Vascular dementia (VaD) is related to hypertension and atherosclerosis and detailed description of its pathogenesis is outside the scope of this review. The importance of age as the main risk factor raises basic questions about the relationship of these diseases to the ageing process itself. Similarities and differences between ageing and disease may be important for a rational approach to prevention and treatment of cognitive decline and dementia in later life.
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PMID:Some developments in brain ageing and dementia. 949 98

Many long-term care residents are diagnosed with dementia, but dementia appears in many forms. Alzheimer's disease, the most common, is typified by a slow onset and relentless progression to complete incapacitation. Vascular dementia usually appears somewhat abruptly, is associated with vascular comorbidities, and has an unpredictable progression pattern. Lewy body dementia shares features of both Alzheimer's and Parkinson's disease; its hallmarks include fluctuating cognitive performance, visual hallucinations, and extrapyramidal motor symptoms. Frontotemporal dementias are associated less with memory disorders and more with behavioral and language aberrations. Mixed dementia covers those patients who do not have an apparent singular cause of dementia. Pseudodementia is a dementia resulting from underlying causes and is reversible, unlike the aforementioned dementias.
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PMID:Differentiating dementias in long-term care patients. 1736 50

The neurocognitive and behavioral profiles of vascular dementia and vascular cognitive impairment, dementia with Lewy bodies and Parkinson's disease with dementia, and dementia syndromes associated with frontotemporal lobar degenerations are compared and contrasted with Alzheimer's dementia (AD). Vascular dementia/vascular cognitive impairment is characterized by better verbal memory performance, worse quantitative executive functioning, and prominent depressed mood. Dementia with Lewy bodies and Parkinson's disease with dementia are equally contrasted with AD by defective processing of visual information, better performance on executively supported verbal learning tasks, greater attentional variability, poorer qualitative executive functioning, and the presence of mood-congruent visual hallucinations. The frontal variant of frontotemporal lobar degeneration (frontotemporal dementia) differs from AD by better multimodal retention on learning tasks, different patterns of generative word fluency, defective qualitative executive functioning, and by markedly impairment of comportment. For temporal variants of frontotemporal lobar degenerations, progressive aphasia and semantic dementia, worse language performance relative to AD is typically characteristic.
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PMID:Cognitive-behavioral profiles of neurodegenerative dementias: beyond Alzheimer's disease. 1800 9

The aim of this study is to investigate the frequency, causes, and clinical characteristics of individuals with presenile dementia with an age of onset less than 65 years. A staged questionnaire survey was performed among all hospitals and clinics, all faculties of care and welfare services, and all local governmental offices in Aichi prefecture. The response rate of the primary survey was 62.3%, and that of the secondary survey was 90.1%. The number of people with presenile dementia after adjusting for duplicated subjects was 1,092 (569 men, 520 women and 3 of unknown gender). The average age was 60.7 +/- 7.1 (mean +/- SD) years, and age of onset was 55.1 +/- 7.8 years. Vascular dementia (VD) was the most frequent cause in men (42.2%), followed by Alzheimer's disease (AD: 24.8%), frontotemporal dementia (FTD: 4.6%) and Parkinson disease (PD: 3.8%). In women, AD was the most common (45.8%), followed by VD (25.4%), FTD (7.4%) and PD (3.4%). Overall, AD and VD were the most common causes of presenile dementia, followed by FTD and PD. The highest prevalence of presenile dementia was seen in the age range of 60- 64-years-old. This was true for both men and women.
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PMID:[Frequency and clinical characteristics of individuals with presenile dementia in Aichi prefecture]. 1961 42

Dementia is a common illness with an incidence that is rising as the aged population increases. There are a number of neurodegenerative diseases that cause dementia, including Alzheimer's disease, dementia with Lewy bodies, and frontotemporal dementia, which is subdivided into the behavioral variant, the semantic variant, and nonfluent variant. Numerous other neurodegenerative illnesses have an associated dementia, including corticobasal degeneration, Creutzfeldt-Jakob disease, Huntington's disease, progressive supranuclear palsy, multiple system atrophy, Parkinson's disease dementia, and amyotrophic lateral sclerosis. Vascular dementia and AIDS dementia are secondary dementias. Diagnostic criteria have relied on a constellation of symptoms, but the definite diagnosis remains a pathologic one. As treatments become available and target specific molecular abnormalities, differentiating amongst the various primary dementias early on becomes essential. The role of imaging in dementia has traditionally been directed at ruling out treatable and reversible etiologies and not to use imaging to better understand the pathophysiology of the different dementias. Different brain imaging techniques allow the examination of the structure, biochemistry, metabolic state, and functional capacity of the brain. All of the major neurodegenerative disorders have relatively specific imaging findings that can be identified. New imaging techniques carry the hope of revolutionizing the diagnosis of neurodegenerative disease so as to obtain a complete molecular, structural, and metabolic characterization, which could be used to improve diagnosis and to stage each patient and follow disease progression and response to treatment. Structural and functional imaging modalities contribute to the diagnosis and understanding of the different dementias.
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PMID:Neuroimaging in dementia. 2127 88

Presenile Dementia or Early Onset Dementia (EOD) is a public health problem, it differs from Senile Dementia, and encloses a significant number of cases; nevertheless, it is still poorly understood and underdiagnosed. This study aims to review the prevalence and etiology of EOD, comparing EOD with Senile Dementia, as well as to show the main causes of EOD and their prevalence in population and non-population based studies. The computer-supported search used the following databases: Pubmed/Medline, ISI Web of Knowledge and Scielo. The search terms were alcohol-associated dementia, Alzheimer's disease, dementia, Creutzfeldt-jakob disease, dementia with lewy bodies, early onset dementia, frontotemporal lobar degeneration, Huntington's disease, mixed dementia, neurodegenerative disorders, Parkinson's disease dementia, presenile dementia, traumatic brain injury, vascular dementia. Only papers published in English and conducted from 1985 up to 2012 were preferentially reviewed. Neurodegenerative diseases are the most common etiologies seen in EOD. Among the general population, the prevalence of EOD was found to range between 0 to 700 per 100.000 habitants in groups of 25-64 years old, with an increasing incidence with age. The progression of EOD was found to range between 8.3 to 22.8 new cases per 100.000 in those aged under 65 years. Alzheimer's disease (AD) is the major etiology, followed by Vascular Dementia (VaD) and Frontotemporal Lobar Degeneration (FTLD). A larger number of epidemiological studies to elucidate how environmental issues contribute to EOD are necessary, thus, we can collaborate in the planning and prevention of services toward dementia patients.
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PMID:Epidemiology of early-onset dementia: a review of the literature. 2387 13

The natural aging process brings about some inevitable consequences, such as olfactory dysfunction, which is also frequently linked to numerous neurodegenerative disorders. Many age-related dementia, such as Alzheimer's disease, Vascular dementia, Parkinson's disease, and Frontotemporal Dementia often display olfactory dysfunction. Despite the overwhelming evidence of above mentioned facts, the symptomatic relevance and potential clinical and pre-clinical value of olfactory dysfunction remains overlooked by many clinicians and public alike. Olfactory dysfunction has strong practical implications on daily activities and, although not as prominent as in other mammals, olfaction is still an evolutionarily relevant sense involved in human survival (e.g., smelling gas; bad food). In this work, we provide a brief review of current research related to the olfactory dysfunction profiles in different types of dementia. Additionally, we present a compilation of accessible, easy to use olfaction assessment tools; and highlight future directions in terms of improving clinical diagnosis in patient care and research.
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PMID:Olfactory dysfunction in dementia. 2540 89

Neurodegenerative diseases represent a large group of neurological disorders with heterogeneous clinical and pathological profiles. The majority of current therapeutic strategies provide temporary symptomatic relief but do not target the underlying disease pathobiology and thus do not affect disease progression. G protein-coupled receptors (GPCRs) are among the most successful targets for therapeutic development of central nervous system (CNS) disorders. Many current clinical therapeutic agents act by targeting this class of receptors and downstream signaling pathways. Here, we review evidence that perturbation of GPCR function contributes to the pathophysiology of various neurodegenerative diseases, including Alzheimer's disease, Frontotemporal dementia, Vascular dementia, Parkinson's disease, and Huntington's disease.
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PMID:The role of GPCRs in neurodegenerative diseases: avenues for therapeutic intervention. 2828 70


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