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Late-onset

A (Hex A) catalyzing the biodegradation of gangliosides. Accumulation of gangliosides in lysosomes primarily affects brain neurons. In the early onset form of the disease, children become blind, deaf, and unable to swallow. Children die usually before the age of three. A late onset form ofthe disease occurs in young adults and is usually nonfatal. [Pg.558]

SorLA Polymorphisms (sporadic) Late-onset Alzheimer s disease... [Pg.706]

Late-onset centronuclear myopathies show a predominance of limb-girdle and truncal muscle weakness with only rare facial or eye involvement. Although this group is classified with the congenital myopathies, weakness only becomes appar-... [Pg.294]

Figure 6. Glycogen storage in acid maltase (AM) deficiency in this late-onset case not all muscle fibers are affected. Figure 6. Glycogen storage in acid maltase (AM) deficiency in this late-onset case not all muscle fibers are affected.
J Clin Psychopharmacol 23 294-304, 2003a Kranzler HR, Pierucci-Lagha A, Feinn R, et al Effects of ondansetron in early- vs late-onset alcoholics a prospective, open-label study. Alcohol Clin Exp Res 27 1150-1155, 2003b... [Pg.48]

Acne vulgaris typically begins around puberty and early adolescence it tends to present earlier in females, usually at about 12 or 13 years, than in males, 14 or 15 years, due to later onset of puberty in males. Acne has been estimated to affect 95-100% of 16- to 17-year-old boys and 83-85% of 16- to 17-year-old girls. Acne settles in the vast majority by 23-25 years of age, persisting for longer in some 7% of individuals 1% of males and 5% of females exhibit acne lesions at 40 years of age. There is a small group of individuals who develop late-onset acne, beyond the age of 25 years. [Pg.113]

De Reuck J, Goethals M. Claeys I, Van Maele G, De Clerck M, EEG findings after a cerebral territorial infarct in patients who develop early- and late-onset seizures. Eur Neurol 2006 55(4) 209-213. [Pg.195]

One of the most likely risk factors for AzD is the patient s genotype for apolipoprotein E (ApoE), which is believed normally to be involved in neuronal repair and growth, but is also found in plaques and tangles. Three distinct forms of ApoE, E2, E3 and E4 are encoded on chromosome 19 but it is the ApoE, E4 allele that occurs at a much higher frequency in late-onset AzD patients (50%) compared with controls (16%) and binds to and possibly increases the formation of )S-amyloid. Many early-onset cases... [Pg.378]

Diabetes is a metabolic disorder where glucose metabolism in the body is impaired. Type 1 diabetes is an early onset disease in which the pancreatic cells lose the function of insulin secretion either by genetic disposition or by a viral attack. Type 2 diabetes is a late onset disease developed due to insufficient insulin secretion or insulin resistance resulting in impaired glucose metabolism. [Pg.367]

Unless risk factors for infection owing to potentially antibiotic-resistant bacteria ° Late-onset hospital-acquired pneumonia... [Pg.127]

Dementia of the Alzheimer s type (early- or late-onset)... [Pg.514]

The genetic basis for the more common late-onset AD appears more complex. Genetic susceptibility is more sporadic and it may be more dependent on environmental factors.9 The apolipoprotein E (apo E) gene on chromosome 19 has been identified as a strong risk factor for late-onset AD. There are three variants of apo E however, carriers of two or more of the apo E4 allele have an earlier onset of AD (approximately 6 years earlier) compared with non-carriers.9 Only 50% of AD patients have the apo E4 allele, thus indicating it is only a susceptibility marker. [Pg.515]

Some regimens are designed for outpatient administration over much longer time periods and have been used, for example, with allopurinol dermal reactions. Such late-onset morbiliform reactions, sometimes overlapping with erythema multiforme minor, are difficult to evaluate because it is often unclear to what extent the patients were at risk for recurrent reaction. [Pg.827]

List the common pathogens that cause community-acquired pneumonia, aspiration pneumonia, ventilator-associated pneumonia (early versus late onset), and health care-associated pneumonia. [Pg.1049]

Hospital (Late onset and/or risk factors for resistant... [Pg.1050]

TABLE 68-4. Empirical Therapy for Late-Onset HAP, HCAP, or VAP... [Pg.1058]

Health care-associated, ventilator-associated, or nosocomial pneumonia (Late onset and/or MDR pathogen risk factors) Antipseudomonal penicillin OR Antipseudomonal cephalosporin OR Antipseudomonal carbapenem plus Aminoglycoside OR Antipseudomonal fluoroquinolone plus Vancomycin or linezolid... [Pg.1191]

Jeste, Dilip V., Kelly A. Harless and Barton W. Palmer. Chronic late-onset schizophrenia-like psychosis that remitted revisiting Newtons psychosis Amer J Psychiatry 157 (Mar 2000) 444-449. rhttp //aip.psvchiatryonline.org/cgi/content/full/l 57/3/4441. [Pg.274]

In 1993/1994 a series of publications caused a stir in the AD research community, since for the first time they linked a specific neuropathological process in late-onset AD to a genetic marker. Researchers looking at the composition of plaques found that the protein apolipoprotein E (ApoE) was associated with p-amyloid in the cerebrospinal fluid (CSF) of AD patients (Strittmatter et al., 1993). The gene for ApoE is on the same human chromosome (number 19) which was a risk factor in some AD pedigrees. The gene for ApoE comes in three versions (alleles) Apo s2, Apo s3 and, most importantly, Apo s4 these result in three slightly different variants of the protein. Humans carry two versions of the allele and so can have none, one or two of any of the versions of the Apo... [Pg.198]

Extrapyramidal side effects These are caused by antipsychotic drugs. They are characterised by motor and postural disturbances, of which the most serious is late-onset tardive dyskinesia. [Pg.242]

Corder EH, Saunders AM, Strittmatter WJ, Schmechel DE, Gaskell PC, Small GW, Roses AD, Haines JL and Pericak-Vance MA (1993). Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer s disease in late onset families. Science, 261, 921-923. [Pg.261]

Saunders AM, Strittmatter WJ, Schmechel D, George-Hyslop PH, Pericak-Vance MA, Joo SH, Rosi BL, Gusella JF, Crapper-MacLachlan DR, Alberts MJ et al. (1993). Association of apolipoprotein E allele epsilon 4 with late-onset familial and sporadic Alzheimer s disease. Neurology, 43, 1467-1472. [Pg.282]

Strittmatter WJ, Saunders AM, Schmechel D, Pericak-Vance M, Enghild J, Salvesen GS and Roses AD (1993). Apolipoprotein E High-avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial Alzheimer disease. Proceedings of the National Academy of Science USA, 90, 1977-1981. [Pg.284]

LaMonte, B. H., Wallace, K. E., Holloway, B. A. et al. Disruption of dynein/dynactin inhibits axonal transport in motor neurons causing late-onset progressive degeneration. Neuron 34 715-727,2002. [Pg.501]

APOE is the only established late-onset Alzheimer s disease gene 656 Other late-onset Alzheimer s disease loci 656... [Pg.653]


See other pages where Late-onset is mentioned: [Pg.241]    [Pg.360]    [Pg.708]    [Pg.292]    [Pg.294]    [Pg.298]    [Pg.323]    [Pg.32]    [Pg.248]    [Pg.127]    [Pg.639]    [Pg.998]    [Pg.1049]    [Pg.1055]    [Pg.1057]    [Pg.1351]    [Pg.145]    [Pg.251]    [Pg.95]    [Pg.142]    [Pg.412]    [Pg.337]    [Pg.330]    [Pg.635]   
See also in sourсe #XX -- [ Pg.15 ]




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Genetic diseases late-onset

Late-onset blindness

Late-onset nosocomial pneumonia

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