Cognitive Impairment in Mild General Paresis of the Insane: AD-Like Pattern
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<i>Background/Aims:</i> We investigated the clinical and cognitive features of patients with mild general paresis of the insane (GPI) in comparison to Alzheimer’s disease (AD) patients, mild frontotemporal dementia (FTD) patients and normal elderly individuals. <i>Methods:</i> Twelve patients with mild GPI, 24 patients with mild AD, 11 patients with mild FTD and 36 healthy subjects participated in the current study. A comprehensive neuropsychological battery was used to assess memory, language, attention, executive function, visuospatial ability, etc. In addition, cranial MRI were also obtained from the 3 patient groups. <i>Results:</i> Mild GPI showed a similar pattern of cognitive impairments in memory, language and executive function to mild AD, but a mixed pattern of dissimilarities to mild FTD. Mild GPI patients had more complaints and positive signs in the nervous system than mild AD patients, and cranial MRI results showed that mild GPI patients usually had atrophy of the medial temporal lobe. <i>Conclusion:</i> There is an overall decline in cognitive functions of mild GPI patients, which is comparable to that in AD patients, suggesting that there is a wide range of structural changes in the brains of mild GPI patients as well. However, further studies are needed to verify whether these structural changes are similar to those in AD.Keywords:
Frontal lobe
Paresis
Frontotemporal lobar degeneration
Frontotemporal lobar degeneration
Semantic dementia
Nosology
Corticobasal degeneration
Neuropsychiatry
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Frontotemporal lobar degeneration
Executive dysfunction
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Frontotemporal lobar degeneration
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Frontotemporal lobar degenerations are clinically, genetically, and molecularly heterogeneous diseases characterized by mainly frontal and temporal atrophy and affecting behavioral, language, cognitive, and motor functions. The term frontotemporal dementia incorporates 3 distinct clinical syndromes seen in frontotemporal degenerations: behavioral variant of frontotemporal dementia, progressive nonfluent aphasia, and semantic dementia. Progressive supranuclear palsy syndrome, corticobasal syndrome, and motor neuron disease syndrome are also associated with frontotemporal lobar degenerations. The neuropathologic hallmark of frontotemporal lobar degenerations is accumulation of abnormal proteins in the cytoplasm and nuclei of neurons and glial cells. Proteins involved in pathologic processes that represent the basis for frontotemporal lobar degeneration classification are tau protein, transactive response DNA-binding protein of 43 kDa, and "fused in sarcoma" protein. The aim of this review is to provide a summary of practical approaches for neuropathologic diagnostics of the rapidly evolving classifications of frontotemporal lobar degenerations.
Frontotemporal lobar degeneration
Semantic dementia
Corticobasal degeneration
Primary progressive aphasia
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Frontotemporal lobar degeneration
Semantic dementia
Primary progressive aphasia
Degeneration (medical)
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Frontotemporal dementia (FTD) is an uncommon but important form of degenerative disease characterized by clinical syndromes that result from degeneration of the frontal and temporal lobes. FTD is divided based on clinical presentation into behavioral variant FTD (bvFTD), semantic dementia, and progressive nonfluent/agrammatic aphasia. Several recent studies have advanced our knowledge of the genetics of FTD, with the three most common FTD genes being microtubule-associated protein tau (MAPT) and progranulin (GRN), and a noncoding repeat expansion in C9ORF72. Tau and TDP-43 are the most common pathologies associated with FTD. No pharmacological therapies are currently approved for use in FTD.
C9ORF72
Frontotemporal lobar degeneration
Semantic dementia
Primary progressive aphasia
Tauopathy
Corticobasal degeneration
Tau protein
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Frontotemporal lobar degeneration
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Research into the non-Alzheimer dementias has exploded over the last 2 decades, and frontotemporal lobar degeneration has emerged as the most common cause of dementia in patients below the age of 65. In 1998, an international consortium of investigators focusing on this disease entity met and agreed upon the classification of 3 subtypes of frontotemporal lobar degeneration, using regional atrophy to distinguish them. These are: a frontally predominant form called frontotemporal dementia, a temporally predominant form called semantic dementia, and a left-frontally predominant syndrome, called progressive nonfluent aphasia. With the rise of genetic and neuropathologic findings, however, the usefulness of this subtype classification has been called into question. This paper discusses the major pertinent findings, and the implications of classifying the disease on the basis of atrophy versus genetic or molecular mechanisms.
Semantic dementia
Frontotemporal lobar degeneration
Primary progressive aphasia
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Frontotemporal dementia is the second most common early onset dementia after Alzheimer disease. Frontotemporal dementias are a complex group of dementias. The clinical diagnosis can be perplexing because of concurring psychiatric and neurologic syndromes. Frontotemporal lobar degeneration, the underlying pathology, represents an emerging group of proteinopathies. Genetic factors play an important part in the etiologies of dementias. This article overviews current defining characteristics of frontotemporal dementias known also as frontotemporal lobar degenerations.
Frontotemporal lobar degeneration
Semantic dementia
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Approximately 15% of patients with frontotemporal dementia (FTD) have co-occurring motor neuron disease (MND). FTD-MND cases have frontotemporal lobar degeneration (FTLD)–transactive response DNA-binding protein (TDP) pathology, which is divided into four subtypes (types A, B, C, and D) based on the morphological appearance, cellular location, and distribution of the abnormal TDP inclusions and dystrophic neurites. We report a patient with FTD-MND whose pathological diagnosis was FTLD-TDP type B. This is the first documented autopsy-confirmed case of FTD-MND in Korea. Key Words: Frontotemporal dementia, Motor neuron disease, Transactive response DNA-binding protein
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