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.