Myoclonus, Seizures, and Paratonia in Alzheimer Disease

Risse, Steven C.; Lampe, Thomas H.; Bird, Thomas D.; Nochlin, David; Sumi, S. M.; Keenan, Trisha; Cubberley, Lyndel; Peskind, Elaine R.; Raskind, Murray A.

doi:10.1097/00002093-199040400-00003

Cited by 101 publications

(67 citation statements)

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“…Neuropathologic studies of the AD3 families have shown extensive senile plaques, NFTs, and granulovacuolar changes in the hippocampus. Amyloid deposits in the cerebellum were a more variable feature and were not observed in all patients autopsied (83,(88)(89)(90). In summary, the clinical and neuropathologic phenotype of AD3 families overlaps those observed in other forms of AD.…”

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confidence: 79%

“…The clinical features characteristic of AD in these families include prominent seizures, myoclonus, and paratonia, which have been observed in many of the sub- jects from different families (81,83,87,88). These features are more variable, occurring later in the course of the disease in other forms of AD (89,90). The exception in the AD3 kindreds may be the SNW/FAD3 family (88), in which extrapyramidal signs, seizures, and myoclonus were not observed (82).…”

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confidence: 99%

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Genetic dissection of Alzheimer disease, a heterogeneous disorder.

Schellenberg

1995

Proc. Natl. Acad. Sci. U.S.A.

166

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The genetics of Alzheimer disease (AD) are complex and not completely understood. Mutations in the amyloid precursor protein gene (APP) can cause early-onset autosomal dominant AD. In vitro studies indicate that cells expressing mutant APPs overproduce pathogenic forms of the A beta peptide, the major component of AD amyloid. However, mutations in the APP gene are responsible for 5% or less of all early-onset familial AD. A locus on chromosome 14 is responsible for AD in other early-onset AD families and represents the most severe form of the disease in terms of age of onset and rate of decline. Attempts to identify the AD3 gene by positional cloning methods are underway. At least one additional early-onset AD locus remains to be located. In late-onset AD, the apolipoprotein E gene allele epsilon 4 is a risk factor for AD. This allele appears to act as a dose-dependent age-of-onset modifier. The epsilon 2 allele of this gene may be protective. Other late-onset susceptibility factors remain to be identified.

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confidence: 79%

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confidence: 99%

Genetic dissection of Alzheimer disease, a heterogeneous disorder.

Schellenberg

1995

Proc. Natl. Acad. Sci. U.S.A.

166

View full text Add to dashboard Cite

show abstract

“…Furthermore, the incidence has been shown to increase with age in the Nordic population [21][22][23]. The reported prevalence of EP in dementia and AD varied from 5% to 64% [24][25][26][27][28][29][30][31][32][33][34]. When all cognitively unimpaired subjects with HS were lumped together here, three out of 23 (11%) had displayed EP during life, thus indicating a high frequency, when compared to the general population.…”

Section: Discussionmentioning

confidence: 88%

Hippocampal Sclerosis and Epilepsy in Elderly Population

Rauramaa¹,

Solomon²,

Pikkarainen³

et al. 2017

J Alzheimers Dis Parkinsonism

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“…The 1% prevalence of epilepsy in the general population increases to 8% in DS, 10% in AD (Menendez, 2005;Risse et al, 1990;Velez and Selwa, 2003), and 33% in autism . The interpretation of developmental changes in autism has been challenged by the need to differentiate among lesions that are not associated with epilepsy, that cause epilepsy, and that are produced by epilepsy (Sutula and Pitkanen, 2001).…”

Section: Epilepsy-associated Pathologymentioning

confidence: 98%

Characterization of the Pathological and Biochemical Markers that Correlate to the Clinical Features of Autism: The Neuropathological Markers of Abnormal Brain Development and Aging in Autism

Wısnıewskı¹

2010

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Myoclonus, Seizures, and Paratonia in Alzheimer Disease

Cited by 101 publications

References 0 publications

Genetic dissection of Alzheimer disease, a heterogeneous disorder.

Genetic dissection of Alzheimer disease, a heterogeneous disorder.

Hippocampal Sclerosis and Epilepsy in Elderly Population

Characterization of the Pathological and Biochemical Markers that Correlate to the Clinical Features of Autism: The Neuropathological Markers of Abnormal Brain Development and Aging in Autism

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