Sentences with phrase «of amyloid precursor»

One hypothesis is that as a regulator of Amyloid Precursor Protein (APP), a gene that may be partly responsible for inducing Alzheimer's, TSH levels may have a direct impact on the prevalence of Alzheimer's.

The main constituents of extracellular amyloid plaque, amyloid β40, 42, is produced by the cleavage of amyloid precursor protein (APP).»

Aβ results from the normal cleavage of amyloid precursor protein (APP), but its accumulation and aggregation into plaques represents the quintessential feature of AD.27 Aβ is found in orders of magnitude greater in AD brains than in healthy brains.28 This fact is noteworthy because lower concentrations of Aβ tend to stay soluble; higher concentrations form plaques more readily.29

Beta amyloid plaques can form when particular fragments of the amyloid precursor protein (APP), cleaved by the enzyme gamma secretase, clump together.

The production of neurotoxic Aβ peptide results from the specific proteolytic processing of the amyloid precursor protein (APP).

These studies revealed that loss of NEU1 activity was associated with a build - up in lysosomes of the amyloid precursor protein (APP), which they identified as a natural target of the enzyme.

Our microscopy studies with quantitative co-localization analysis revealed the presence of intraneuronal Aβ in transgenic rats, with an immunological signal that was clearly distinguished from that of the amyloid precursor protein (APP) and its C - terminal fragments (CTFs).

Amyloid beta (Aβ) is a small peptide molecule generated from cleavage of amyloid precursor protein (APP).

Increasing evidence suggests that the synaptic functions of the amyloid precursor protein (APP), that is key to Alzheimer (AD) pathogenesis, may be carried out by its secreted ectodomain.

Specifically, that aggregates of A-beta peptides, which are formed following cleavage of the Amyloid Precursor Protein (APP), instigate a series of events that leads to neurodegeneration and, eventually, AD.

Role of amyloid precursor protein (APP) in brain development and implications for Down syndrome

Exploiting this compartmentalization, the team developed an endosomally - targeted β - secretase inhibitor that specifically blocked cleavage of amyloid precursor protein but not non-amyloid proteins.

Previously, researchers have shown that treating cells with neuregulin - 1, for example, dampens levels of amyloid precursor protein, a molecule that generates amyloid beta, which aggregate and form plaques in the brains of Alzheimer's patients.

That's because the boosted mice produced normal — rather than high — levels of the amyloid precursor proteins from which plaques are made.

Not exact matches

This protein is part of the enzymatic engine that churns out amyloid beta — a key molecular culprit in Alzheimer's disease — by snipping it out of a larger precursor protein called APP.

Specifically, rodents genetically modified to express human amyloid precursor protein (hAPP), which can lead to the debilitating plaques that form in the brains of Alzheimer's patients, seem to struggle to find the hidden platform relative to their healthy peers.

IRON overload may accelerate Alzheimer's disease, according to research that also reveals the role of beta - amyloid precursor protein (APP), which forms plaques in affected brains.

«What's distinct here is a regulatory role whereby the prion protein inhibits production of amyloid beta peptide from its precursor protein,» says Millhauser.

In the current study, a collaborative team of researchers at the Gladstone Institute and the Baylor College of Medicine in Houston, created a strain of mice that overproduces a precursor of Aβ known as amyloid precursor protein.

On page 735, molecular biologists describe a new candidate for b - secretase, an elusive enzyme that is needed to free one end of b - amyloid from its larger precursor protein.

In their latest research, Lawrence Rajendran, of the University of Zurich in Switzerland, and his colleagues discovered that, unlike non-amyloid proteins, the Alzheimer's - associated amyloid precursor protein is cleaved by β - secretase in membrane - bound compartments inside cells, called endosomes.

In the brains of patients with Alzheimer's disease (AD), amyloid precursor protein is broken apart, and the resulting fragments — β - amyloid peptides, or Aβ peptides — aggregate to form plaques.

A plaque is an accumulation of proteins that are primarily made up of Amyloid beta (A-beta), a small structure that splits off from the Amyloid Precursor Protein (APP).

An illustration of how swapping an amino acid in beta amyloid precursor proteins results in longer and shorter strands (Credit: Brian Kladko and Weihong Song / University of British Columbia)

The mutations take place on a protein that serves as the precursor for amyloid beta, a different protein that forms plaques in the brains of individuals afflicted by Alzheimer's disease.

Then, in 1987, Tanzi and his colleagues published their discovery of the first Alzheimer's - associated gene, which leads to the formation of amyloid - beta precursor protein, or APP.

The TOMM40 gene encodes a barrel - shaped protein in the outer membrane of mitochondria that forms a channel for molecules — including the precursor to amyloid — to enter.

An illustration of how swapping an amino acid in beta amyloid precursor proteins results in longer and shorter strands

One interesting hypothesis by the study authors looks at the role that thyroid hormone plays in regulating the expression of a gene called the amyloid precursor protein (APP), which has a role in Alzheimer's.

Classical hallmarks of Alzheimer's disease (AD) are a synaptic loss, cholinergic neuron death, and abnormal protein deposition, particularly of toxic amyloid - β peptide (Aβ) that is derived from amyloid - β protein precursor (AβPP) by the action of beta - and gamma - secretases.

Other work addresses mechanisms for decreasing amyloid beta biosynthesis by enhancing cleavage of its precursor protein by the alpha - secretase enzyme.

Abstract: Classical hallmarks of Alzheimer's disease (AD) are a synaptic loss, cholinergic neuron death, and abnormal protein deposition, particularly of toxic amyloid - β peptide (Aβ) that is derived from amyloid - β protein precursor (AβPP) by the action of beta - and gamma - secretases.

Proteolytic cleavage of amyloid - β - protein precursor (AβPP) by β - and γ - secretases results in production of the amyloid - β peptide (Aβ) that accumulates in the brains of sufferers of Alzheimer's disease (AD).

There were no differences in CSF levels of total tau, Aβ42, Aβ40, soluble amyloid β protein precursor (sAβPP) α or β, or F2 - isoprostanes.

Aged mutant amyloid precursor protein mice with established disease showed a near complete restoration in levels of synaptic and neuronal proteins after exposure to young blood in parabiosis (synaptophysin P =.02; calbindin P =.02) or following intravenous plasma administration (synaptophysin P <.001; calbindin P =.14).

Using blood collected from elderly persons aged up to one hundred and demonstrating no cognitive impairment, the researchers isolated precisely those immune cells whose antibodies are able to identify toxic beta - amyloid plaques but not the amyloid precursor protein that is present throughout the human body and that presumably plays an important role in the growth of nerve cells.

Overexpression of human amyloid - β protein precursor (AβPP) within the gut was assessed by qPCR and IHC; fecal microbiome analysis was conducted by 16SrRNA quantitation of selected phyla and species.

There exist several dozen lines of transgenic mice that express human amyloid - β protein precursor (AβPP) with Alzheimer's disease (AD)- linked mutations.

Beta amyloid is a fragment of a protein snipped from another protein called amyloid precursor protein (APP).

The amyloid - β protein precursor (AβPP) is cleaved by a transmembrane protease termed β - site AβPP cleavage enzyme (BACE1), which is being explored as a target for therapy and prevention of Alzheimer's disease (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

Baiping Wang, Zilai Wang, Lu Sun, Li Yang, Hongmei li, Allysa Cole, Jennifer Rodriguez - Rivera, Hui - Chen Lu, Hui Zheng (2014) «The Amyloid Precursor Protein Controls Adult Hippocampal Neurogenesis through GABAergic Interneurons», Journal of Neuroscience 34:13314 - 25.

Generation and Characterization of Mutant Cell Lines Defective in -LCB- gamma -RCB-- Secretase Processing of Notch and Amyloid Precursor Protein

17 / Jun / 2013 Although a family history of Alzheimer's disease is a primary risk factor for the devastating neurological disorder, mutations in only three genes — the amyloid precursor protein and presenilins 1 and 2 — have been established as causative for inherited, early - onset Alzheimer's, accounting for about half of such cases.

Evidence shows that green tea may possess potent activities of neuroprotection and amyloid precursor protein processing leading to cognitive enhancement.

Understanding the role of soy constituents, such as daidzein, on AβPP (amyloid - β protein precursor) synthesis and metabolism and modulation of intake during pregnancy and infancy could reduce seizure incidence and prevent neurological damage.»

Stimulation of beta - amyloid precursor protein trafficking by insulin reduces intraneuronal beta - amyloid and requires mitogen - activated protein kinase signaling.