Sentences with phrase «brain atrophy by»

The new approach, published today in the International Journal of Stroke, can quantify visible brain injury from cerebral small vessel disease (SVD) and brain atrophy by translating the million plus bits of information stored in brain scans into a single measure, the «brain health index.»

Not exact matches

To quote Napoleon Hill, «A good shock often helps the brain that has been atrophied by habit.»
Or has the American collective brain atrophied to such a pathetic state where any idiot can be elected just by mentioning the word «abortion»?
The disease is caused by a genetic mutation that leads to abnormal clumps of protein in the brain, eventually resulting in the atrophy and death of nerve cells.
Recent studies suggest that the total loss in brain volume due to atrophy — a wasting away of tissue caused by cell degeneration — between our teen years and old age is 15 percent or more, which means that by the time we're in our seventies, our brains have shrunk to the size they were when we were between 2 and 3 years old.
But I can still write a pretty good sentence, heartened that the cognitive decline that might be expected to accompany the brain's atrophy is neither linear nor predictable, partly because older brains compensate by forging workarounds in connectivity.
«It was particularly exciting to see plasticity in the neurons impaired by mHTT,» said Davidson, noting that in the HD mice, brain areas that had begun to atrophy recovered volume and permitted better motor function after the researchers restored mTORC1 activity to more normal levels.
Previous research by the Northwestern group provided tantalizing clues, showing that SuperAgers have distinctive brain features: thicker cortexes, a resistance to age - related atrophy and a larger left anterior cingulate (a part of the brain important to attention and working memory).
He also cited neuroimaging studies showing that prolonged periods of reduced audio stimulation can lead to faster rates of atrophy, changing the brain's structure Additionally, social isolation caused by hearing loss may contribute to further brain decline, Lin said.
Findings from the MS - STAT trial showed that a high, daily dose of simvastatin was safe, well tolerated, and slowed brain atrophy (shrinkage) by 43 % over two years compared with placebo.
This disorder is marked by the loss of motor neurons in the brain and spinal cord, and atrophy of the frontal and temporal lobes.
mThy1 - AS mice administered only control IgG1 suffered dendritic atrophy (as suggested by reduced staining with MAP2) and synaptic loss (evaluated with postsynaptic density - 95 (PSD - 95) and synaptophysin) across several regions of the brain, but this neurodegenerative damage was substantially prevented in mice administered 1H7, 5C1, or 9E4.
Although most infants had microcephaly by head circumference measure, some patients had a measurement that was consistent with their gestational age, as brain atrophy was compensated by an enlargement in ventricular size.19
The accelerated rate of brain atrophy in elderly with mild cognitive impairment can be slowed by treatment with homocysteine - lowering B vitamins.
Salsalate successfully reversed these effects in a mouse model of FTD, lowering tau levels in the brain, rescuing memory impairments, and protecting against atrophy of the hippocampus — a brain region essential for memory formation that is impacted by dementia.
B vitamin treatment led to a difference in final tHcy concentration of 31.7 % compared with the placebo, and was accompanied by a reduction in the rate of brain atrophy of almost 30 %.
Corticobasal degeneration is a progressive neurological disorder characterized by nerve cell loss and atrophy (shrinkage) of various regions of the brain, including the cerebral cortex and the basal ganglia (which helps to start and control movements, as well as other functions).
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
Additional exploratory objectives include assessing the impact that each compound has on the toxic mutant protein known to cause loss of brain cells in HD, as well as evaluating potential clinical effects and impact on brain atrophy as measured by magnetic resonance imaging (MRI).
New research suggests that people who have had a concussion can experience more memory problems and atrophy in areas of the brain that are typically damaged by the disease if they have those high - risk genes.
«Clinically and cognitively normal individuals with and without AD risk factors, following dietary patterns characterized by high intakes of whole grains, fresh fruits, vegetables, legumes, fish, and low - fat dairy products (which provide higher intakes of vitamin B12, vitamin D, and n - 3 polyunsaturated fatty acids) and by low intakes of refined sugars, French fries, high - fat dairy products, butter, and processed meat, show lower accumulation of Aβ in the brain and higher cerebral glucose metabolism, as evidenced by neuroimaging analysis of gray matter volumes (a marker of brain atrophy), C - Pittsburgh compound B (to measure the accumulation of fibrillar Aβ), and F - fluorodeoxyglucose (to assess brain glucose metabolism.»
Some experts maintain that the amyloid plaques and neurofibrillary tangles (key hallmarks of brain cell atrophy in Alzheimer's Disease) can all be explained by insulin resistance.
Rhonda Patrick, PHD writes «cold exposures increase cold shock proteins including one in the brain that repairs damaged synapses and in muscle prevents atrophy, how a cold - induced catecholamine lowers inflammation and pain by decreasing the levels of 3 inflammatory mediators...» [10] This is very, very interesting stuff and it's grounded in evolutionary science.
Rhonda Patrick, PHD writes «cold exposures increase cold shock proteins including one in the brain that repairs damaged synapses and in muscle prevents atrophy, how cold - induced norepinephrine lowers inflammation and pain by decreasing the levels of 3 inflammatory mediators...» * [9] This is very, very interesting stuff and it's grounded in evolutionary science.
The latter could be caused by the former, but also by other conditions such as progressive supranuclear palsy (a rare brain disorder that destroys nerve cells) or multiple system atrophy (a degenerative condition originating in parts of the brain).
Prone to hives caused by stress or insect bites, cerebellar ataxia - an undefined problem in the part of the brain that controls coordination, PRA (Progressive retinal atrophy)- gradual deterioration of the retina beginning with night blindness and eventually total blindness, allergies, cancer, heart problems, socialization issues, training and hip dysplasia, thyroid problems
This is caused by a parasite that if contracted by the mother could cause significant harm to the fetus including neurological problems, physical problems, retardation, epilepsy, brain atrophy, and blindness.
By not letting the critical thinking parts of our brains atrophy, we can fend off disease and the natural effects of old age that afflict many members of older generations.
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