Tau epitopes in spinal cord neurofibrillary lesions in Chamorros of Guam

Schmidt, Maria Luiza Gava; Garruto, Ralph M.; Chen, J.; Lee, V. M.-Y.; Trojanowski, John Q.

doi:10.1097/00001756-200011090-00005

Cited by 16 publications

(6 citation statements)

References 2 publications

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“…Notably, in both affected individuals, the initial presentation was with acute respiratory failure, and it is likely that the involvement of tegmental medullary neurons, combined with spinal anterior horn cells involvement (data not shown), accounted for this. Although this has been reported,17–19 such profound respiratory problems have not been noted previously. Thus, the possibility of a tauopathy should be considered in unexplained progressive hypoventilation where more common causes have been excluded.…”

Section: Discussionmentioning

confidence: 47%

Elucidation of the relationship between synovitis and bone damage: A randomized magnetic resonance imaging study of individual joints in patients with early rheumatoid arthritis

Conaghan¹,

O’Connor²,

McGonagle³

et al. 2003

Arthritis & Rheumatism

315

184

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Objective. To simultaneously image bone and synovium in the individual joints characteristically involved in early rheumatoid arthritis (RA).Methods. Forty patients with early, untreated RA underwent gadolinium-enhanced magnetic resonance imaging (MRI) of the second through fifth metacarpophalangeal joints of the dominant hand at presentation, 3 months, and 12 months. In the first phase (0-3 months), patients were randomized to receive either methotrexate alone (MTX) or MTX and intraarticular corticosteroids (MTX ؉ IAST) into all joints with clinically active RA. The MTX-alone group received no further corticosteroids until the second phase (3-12 months), when both groups received standard therapy.Results. In the first phase, MTX ؉ IAST reduced synovitis scores more than MTX alone. There were significantly fewer joints with new erosions on MRI in the former group compared with the latter. During the second phase, the synovitis scores were equivalent and a similar number of joints in each group showed new erosions on MRI. In both phases, there was a close correlation between the degree of synovitis and the number of new erosions, with the area under the curve for MRI synovitis the only significant predictor of bone damage progression. In individual joints, there was a threshold effect on new bone damage related to the level of synovitis; no erosions occurred in joints without synovitis.Conclusion. In early RA, synovitis appears to be the primary abnormality, and bone damage occurs in proportion to the level of synovitis but not in its absence. In the treatment of patients with RA, outcome measures and therapies should focus on synovitis.

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Section: Discussionmentioning

confidence: 47%

Elucidation of the relationship between synovitis and bone damage: A randomized magnetic resonance imaging study of individual joints in patients with early rheumatoid arthritis

Conaghan¹,

O’Connor²,

McGonagle³

et al. 2003

Arthritis & Rheumatism

315

184

View full text Add to dashboard Cite

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“…16 Notably, in both affected individuals, the initial presentation was with acute respiratory failure, and it is likely that the involvement of tegmental medullary neurons, combined with spinal anterior horn cells involvement (data not shown), accounted for this. Although this has been reported, [17][18][19] such profound respiratory problems have not been noted previously. Thus, the possibility of a tauopathy should be considered in unexplained progressive hypoventilation where more common causes have been excluded.…”

Section: Discussionmentioning

confidence: 49%

An English kindred with a novel recessive tauopathy and respiratory failure

Nicholl

Greenstone

Clarke

et al. 2003

Annals of Neurology

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We present the clinicopathological features of two siblings from a consanguineous marriage who presented with respiratory hypoventilation and died 10 days and 4 years later, respectively. This disorder showed extensive tau neuropathology, and both had a novel homozygous S352L tau gene mutation. This is the first description of a pathologically proved young-onset tauopathy with apparent recessive inheritance.

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“…Despite that the presence of filamentous aggregates of epitopes of hyperphosphorylated tau protein in the spinal cord is a typical neuropathological finding of Guam ALS/parkinsonism/dementia complex (29–31), SALS has not been associated with tau pathology (15, 17–19). On the contrary, overexpression of the smallest human tau isoform in transgenic mice leads to the appearance of hyperphosphorylated tau and argyrophilic intraneuronal inclusions formed by tau‐immunoreactive filaments in the spinal cord neurons, and induces a clinical picture of motor weakness that resembles ALS (32).…”

Section: Discussionmentioning

confidence: 99%