Sentences with phrase «familial ad»

Abbreviations: Aβ, amyloid β - peptide; AD, Alzheimer's disease; ALS, amyotrophic lateral sclerosis; Ambra1, activating molecule in Beclin -1-regulated autophagy; AMPK, AMP - activated protein kinase; APP, amyloid precursor protein; AR, androgen receptor; Atg, autophagy - related; AV, autophagic vacuole; Bcl, B - cell lymphoma; BH3, Bcl - 2 homology 3; CaMKKβ, Ca2 + - dependent protein kinase kinase β; CHMP2B, charged multivesicular body protein 2B; CMA, chaperone - mediated autophagy; 2 ′ 5 ′ ddA, 2 ′, 5 ′ - dideoxyadenosine; deptor, DEP - domain containing mTOR - interacting protein; DRPLA, dentatorubral pallidoluysian atrophy; 4E - BP1, translation initiation factor 4E - binding protein - 1; Epac, exchange protein directly activated by cAMP; ER, endoplasmic reticulum; ERK1 / 2, extracellular - signal - regulated kinase 1/2; ESCRT, endosomal sorting complex required for transport; FAD, familial AD; FDA, U.S. Food and Drug Administration; FIP200, focal adhesion kinase family - interacting protein of 200 kDa; FoxO3, forkhead box O3; FTD, frontotemporal dementia; FTD3, FTD linked to chromosome 3; GAP, GTPase - activating protein; GR, guanidine retinoid; GSK3, glycogen synthase kinase 3; HD, Huntington's disease; hiPSC, human induced pluripotent stem cell; hVps, mammalian vacuolar protein sorting homologue; IKK, inhibitor of nuclear factor κB kinase; IMPase, inositol monophosphatase; IP3R, Ins (1,4,5) P3 receptor; I1R, imidazoline - 1 receptor; JNK1, c - Jun N - terminal kinase 1; LC3, light chain 3; LD, Lafora disease; L - NAME, NG - nitro - L - arginine methyl ester; LRRK2, leucine - rich repeat kinase 2; MIPS, myo - inositol -1-phosphate synthase; mLST8, mammalian lethal with SEC13 protein 8; MND, motor neuron disease; mTOR, mammalian target of rapamycin; mTORC, mTOR complex; MVB, multivesicular body; NAC, N - acetylcysteine; NBR1, neighbour of BRCA1 gene 1; NOS, nitric oxide synthase; p70S6K, ribosomal protein S6 kinase - 1; PD, Parkinson's disease; PDK1, phosphoinositide - dependent kinase 1; PE, phosphatidylethanolamine; PI3K, phosphoinositide 3 - kinase; PI3KC1a, class Ia PI3K; PI3KC3, class III PI3K; PI3KK, PI3K - related protein kinase; PINK1, PTEN - induced kinase 1; PKA, protein kinase A; PLC, phospholipase C; polyQ, polyglutamine; PS, presenilin; PTEN, phosphatase and tensin homologue deleted from chromosome 10; Rag, Ras - related GTP - binding protein; raptor, regulatory - associated protein of mTOR; Rheb, Ras homologue enriched in brain; rictor, rapamycin - insensitive companion of mTOR; SBMA, spinobulbar muscular atrophy; SCA, spinocerebellar ataxia; SLC, solute carrier; SMER, small - molecule enhancer of rapamycin; SMIR, small - molecule inhibitor of rapamycin; SNARE, N - ethylmaleimide - sensitive factor - attachment protein receptor; SOD1, copper / zinc superoxide dismutase 1; TFEB, transcription factor EB; TOR, target of rapamycin; TSC, tuberous sclerosis complex; ULK1, UNC -51-like kinase 1; UVRAG, UV irradiation resistance - associated gene; VAMP, vesicle - associated membrane protein; v - ATPase, vacuolar H + - ATPase; Vps, vacuolar protein sorting

Data from patients with familial AD with autosomal dominant mutations4 and longitudinal observation of individuals with positive Aβ PET scans and normal cognition led to the observations that amyloid plaque pathology could be present as long as 2 decades prior to the emergence of the first clinical symptoms of AD.

These PS1 mutations, Q222H and M233T, are completely penetrant causing early - onset familial AD as previously reported in these Australian families.

We show that oxidative modifications of ubiquitin carboxyl - terminal hydrolase L1 (UCH - L1), γ - enolase, actin, and dimethylarginine dimethylaminohydrolase 1 (DMDMAH - 1) are present in the brain of familial AD... subjects.

These findings are probably related to the epileptic phenotype of many pedigrees of patients with early - onset familial AD and to the hyperactivation of neuronal networks in patients with sporadic AD and amyloid - positive nondemented subjects.

These unexpected findings may be related to the epileptic phenotype of many pedigrees of patients with early - onset familial AD and to the hyperactivation of neuronal networks in patients with sporadic AD and amyloid - positive nondemented subjects.

Published in Stem Cell Reports, the study investigated the brain cell function of familial AD patients by using stem cell technologies.

Not exact matches

Genetic factors are clearly indicated as evidenced by dominant mutations in three different genes have been identified that account for the small number of cases of familial, early - onset AD.

Familial aggregation studies show that first degree relatives of probands with AD are more likely to have or develop AD compared to relatives of controls.

Conclusions: These initial results suggest that oxidatively modified proteins are important common features in both familial and sporadic AD.

The problem with your particular case would be the marketability when trying to promote it as «great for your adult children» or «let your parents live in the in - law suite» - however you phrase your rental ads, this would violate Fair Housing rules that prohibit discrimination based on familial status.

Fair Housing Act As a member you agree not to post, email, or otherwise make available content that violates the Fair Housing Act by stating, in any notice or ad for the sale or rental of any dwelling, a discriminatory preference based on race, color, national origin, religion, sex, familial status or handicap (or violates any state or local law prohibiting discrimination on the basis of these or other characteristics).