Neuropathology and memory dysfunction in neurodegenerative disease

Testa, Julie A.; Brumback, Roger A.; Baik, Tai-Kyoung; Leech, Richard W.; Cannon, Thomas C.

doi:10.1017/cbo9780511544378.004

Cited by 4 publications

(5 citation statements)

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“…Reduced cholinergic activity is supposed to be the main reason for the cognitive dysfunction in AD [Terry et al, 1994;Testa et al, 1998]. The present results tentatively suggest that the MMN, or at least the frequency MMN, is under cholinergic modulation.…”

Section: Automatic Discrimination and Adsupporting

confidence: 64%

“…Furthermore, a large amount of neurofibrillary tangles and amyloid plaques accumulate in the cerebral cortex including the mesial temporal lobe [Terry et al, 1994;Testa et al, 1998]. These degenerative changes also involve the unimodal auditory cortex while relatively sparing the primary auditory cortex or its vicinity, which is one source of MMN [Hari et al, 1984;Terry et al, 1994;Alho, 1995].…”

Section: Automatic Discrimination and Admentioning

confidence: 99%

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Mismatch Negativity in Aging and in Alzheimer’s and Parkinson’s Diseases

Pekkonen

2000

Audiol Neurotol

136

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Mismatch negativity (MMN) is an auditory event-related potential (ERP) that reflects automatic stimulus discrimination in the human auditory system. By varying the interstimulus intervals (ISIs), the MMN can be used as an index of auditory sensory memory. This paper focuses on MMN findings in aging and in Alzheimer’s (AD) and Parkinson’s diseases (PD). The accumulated data suggest that MMN to duration deviance, unlike MMN to frequency deviance, is reduced in amplitude in aging at short ISIs. The attenuated MMN to frequency deviance observed at long ISIs in elderly subjects seems to be caused by age-related memory trace decay. Existing results suggest that automatic discrimination for the frequency change is not affected in the early phase of AD, whereas the memory trace seems to decay faster in AD patients. The present findings on PD are not as conclusive, although they tentatively suggest deteriorated automatic change detection. The MMN appears to offer an objective tool for studying auditory processing and memory trace decay in different neurological disorders.

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Section: Automatic Discrimination and Adsupporting

confidence: 64%

Section: Automatic Discrimination and Admentioning

confidence: 99%

Mismatch Negativity in Aging and in Alzheimer’s and Parkinson’s Diseases

Pekkonen

2000

Audiol Neurotol

136

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“…Vice versa, his ventricular size corresponds more closely to that of a person of his age than to that of a patient with AD. Furthermore, PP's major cerebellar atrophy opposes the typical characteristics of AD [although non-specific gait disorders are already characteristic for an intermediate stage (Testa et al, 1998)l. Lastly, hippocampal sclerosis starts very early in AD and shows the relatively greatest loss over time (Braak and Braak, 1996;Double et al, 1996;Rasmusson et al, 1996; DeToledo-Morrell er af., 1997), but was not so prominent in PP.…”

Section: Discussionmentioning

confidence: 99%

“…They emphasized that, as a rule, dementias have an insidious onset and a slowly progressive course. (Probable) Alzheimer's disease (AD), the most frequent form of dementia (Testa et al, 1998), is a disease of the aged; even so-called early-onset (familial) AD manifests typically between the ages of 40 and 64 (Giannakopoulos et al, 1996). The earliest occurrence of AD, namely with an onset between 30 and 40 years, has been proposed for the so-called genetic type PS-I (presenilin-1 on chromosome 14) (Lovestone, 1999).…”

Section: Introductionmentioning

confidence: 99%

Severe degenerative cortical and cerebellar atrophy and progressive dementia in a young adult

et al. 2000

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A 32-year-old patient is described who presented with severe cognitive deficits and major cortical and cerebellar atrophy. Investigations included numerous clinical laboratory tests, magnetic resonance imaging, [1*F]2-fluoro-2-deoxy-D-glucose positron emission tomography and detailed neuropsychological examinations. Tests covered mood, intelligence, attention and concentration, language, verbal fluency, various memory abilities, and cognitive flexibility. Furthermore, some experimental testing procedures were applied, such as drawing objects, and transcoding verbal and Arabic numerals. Laboratory findings failed to give any indication for viral, bacterial, genetic or metabolic diseases, or for chronic intoxication. In particular, no presenilin genes were found. Neuroradiology revealed very severe cortical and less severe cerebellar degeneration. In most neuropsychological tests, the patient was greatly impaired. In spite of some inconsistencies at the anatomical and cognitive levels, it is concluded that, in spite of his young age, the patient suffered from an unusual form of Alzheimer's disease.

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“…The declarative, remote memory impairments seen in PD (Venneri et al 1997;Ivory et al 1999), which are characterised by similar memory loss across all decades of life (Testa et al 1998), are of most concern to recall of past exposures. These types of memory deficits are most evident on effort-demanding tasks (Appollonio et al 1994).…”

Section: Cognitive Dysfunction In Pdmentioning

confidence: 99%

Environmental Risk Factors for Parkinson’s Disease

Gorell¹,

Ford²,

Rybicki³

2003

Handbook of Parkinson's Disease

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Parkinson's disease (PD) is a progressive, degenerative, neurological disease. The progressive disability associated with PD results in substantial burdens for those with the condition, their families and society in terms of increased health resource use, earnings loss of affected individuals and family caregivers, poorer quality of life, caregiver burden, disrupted family relationships, decreased social and leisure activities, and deteriorating emotional well-being. Currently, no cure is available and the efficacy of available treatments, such as medication and surgical interventions, decreases with longer duration of the disease. Whilst the cause of PD is unknown, genetic and environmental factors are believed to contribute to its aetiology. Descriptive and analytical epidemiological studies have been conducted in a number of countries in an effort to elucidate the cause, or causes, of PD. Rural residency, farming, well water consumption, pesticide exposure, metals and solvents have been implicated as potential risk factors for PD in some previous epidemiological studies. However, there is substantial disagreement between the results of existing studies. Therefore, the role of environmental exposures in the aetiology of PD remains unclear.The main component of this thesis consists of a case-control study that assessed the contribution of environmental exposures to the risk of developing PD. An existing, previously unanalysed, dataset from a local case-control study was analysed to inform the design of the new case-control study. The analysis results suggested that regular exposure to pesticides and head injury were important risk factors for PD. However, due to the substantial limitations of this existing study, further confirmation of these results was desirable with a more robustly designed epidemiological study. A new exposure measurement instrument (a structured interviewer-delivered questionnaire) was developed for the new case-control study to obtain data on demographic, lifestyle, environmental and medical factors. Prior to its use in the case-control study, the questionnaire was assessed for test-retest repeatability in a series of 32 PD cases and 29 healthy sex-, age-and residential suburb-matched electoral roll controls. High repeatability was demonstrated for lifestyle exposures, such as smoking and coffee/tea Title .

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Neuropathology and memory dysfunction in neurodegenerative disease

Cited by 4 publications

References 0 publications

Mismatch Negativity in Aging and in Alzheimer’s and Parkinson’s Diseases

Mismatch Negativity in Aging and in Alzheimer’s and Parkinson’s Diseases

Severe degenerative cortical and cerebellar atrophy and progressive dementia in a young adult

Environmental Risk Factors for Parkinson’s Disease

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