Newswise — A new study conducted at the University of Haifa and published recently in the Journal of Neuroscience has identified activity of
brain proteins associated with memory impairments in Alzheimer's disease, and has also found that «repairing» this activity leads to an improvement in memory.
A new study conducted at the University of Haifa and published recently in the Journal of Neuroscience has identified activity of
brain proteins associated with memory impairments in Alzheimer's disease, and has also found that «repairing» this activity leads to an improvement in memory.
Research from Washington University School of Medicine in St. Louis, Radboud University Medical Centre in the Netherlands, and Stanford University shows that disrupting just one night of sleep in healthy, middle - aged adults causes an increase in
a brain protein associated with Alzheimer's disease.
Not exact matches
For one, it would give them three specific biological markers to hone in on: The buildup of beta amyloid and tau
proteins, which cause
brain plaques
associated with Alzheimer's, and
brain nerve cell death.
This drug is designed to reduce the build up of a neural
protein in the
brain called alpha - synuclein that is
associated with the disease.
In an interview, the Glasgow - based neurologist described how he had examined sections of
brain tissue in a retired rugby player and found abnormal
proteins associated with head injuries and dementia.
Most groups have focused on detecting
proteins released from dying
brain cells, but those
proteins are not always abundant after injury and often require exotic or proprietary antibodies to measure, said study corresponding author Adam Chodobski,
associate professor (research) of emergency medicine in the Alpert Medical School of Brown University.
As they studied
brain activity in the knockout mice, the researchers also found prominent changes in a receptor in the
brain known as mGluR5 and other
proteins that support the function of neurons and synapses, said co-lead author Xiaoming Wang, M.D., Ph.D., senior research
associate in Duke's department of pediatrics.
One of your biggest discoveries was how addiction affects the D2 receptor, the
protein that determines how sensitive individuals are to the release of the neurotransmitter dopamine, a chemical in the
brain associated with feelings of reward and pleasure.
In the future, studies are aimed at using novel molecular approaches to selectively delete AMPK in specific
brain regions
associated with nicotine dependence to better understand the functional role of this
protein in addiction.
Fruit flies with the mutant form of LRRK2 also had a disrupted microRNA pathway
associated with the gene, and accumulated toxic
proteins that killed motor - coordinating neurons in the
brain.
The idea for Smith's study was inspired by the work of co-author Alena Savonenko, M.D., Ph.D.,
associate professor of pathology, and her colleagues who showed that loss of serotonin neurons was
associated with more
protein clumps, or amyloid, in mouse
brain.
A drug that acts like a growth - promoting
protein in the
brain reduces degeneration and motor deficits
associated with Huntington's disease in two mouse models of the disorder, according to a study appearing November 27 in the Journal of Neuroscience.
At Stanford, a team led by neurobiologist Ben Barres discovered that synapses in the developing
brain produce two other immune
proteins, C1q and C3,
associated elsewhere in the body with complement
proteins, which work in concert with antibodies to destroy invading microbes.
The technology allows scientists in the lab to «light up» and then monitor a
brain protein called alpha - synuclein that has been
associated with Parkinson's.
In the hippocampus and the amygdala, areas of the
brain thought to be
associated with episodic memory, researchers had shown that the chemical signaling agent called glutamate acts like a key in the lock of some of these
protein «flood gates.»
Most people
associate prion diseases with the
brain, although scientists have found abnormal infectious prion
protein in other organs, including the spleen, kidney, lungs and liver.
«As a result, for the first time, we were able to visualize the
protein's location, at minute scale, under physiologic conditions in an intact
brain cell,» noted Chung, who is now Scientific Co-founder and
Associate Director at Yumanity Therapeutics in Cambridge.
Scientists have revealed that
protein clumps
associated with Alzheimer's disease are also found in the
brains of people who have had a head injury.
Taking on Memory For years people have
associated Alzheimer's withamyloid - beta, or A-beta,
proteins, but in a shocking study, researchers have found thatyoung
brains are creating just as much, if not more of the
protein than oldbrains.
When the scientists recently gave mice a single dose of cocaine and looked for signs of autophagy in their
brain cells, they detected autophagy -
associated proteins and changes in vacuoles in adults and in mouse pups whose mothers had received cocaine while pregnant.
James Hewett,
associate professor of biology, and Yifan Gong, a Ph.D. candidate in biology and neuroscience, have co-authored an article in the journal Neuroscience (Elsevier, 2018) about a
protein in the
brain called T - cell intracellular antigen - 1 (TIA - 1).
Specifically, the release of a stress - coping hormone called corticotropin - releasing factor (CRF), which is widely found in the
brain and acts as a neurotransmitter / neuromodulator, is dysregulated in AD and is
associated with impaired cognition and with detrimental changes in tau
protein and increased production of amyloid - beta —
protein fragments that clump together and trigger the neurodegeneration characteristic of AD.
«It seems that their
brain has found a way to compensate for the presence of the
proteins associated with Alzheimer's.»
Twenty - seven of these mutations were in
proteins specifically
associated with the nervous system, including transthyretin, which helps transport glucose across the blood -
brain barrier, and microcephalin, which partly governs
brain and head size.
The team identified 16
proteins that were strongly
associated with
brain shrinkage in people with mild cognitive impairment or Alzheimer's.
Losing just one night of sleep led to an immediate increase in beta - amyloid, a
protein in the
brain associated with Alzheimer's disease, according to a small, new study by researchers at the National Institutes of Health.
Some of these 10
proteins were
associated with tau and amyloid
proteins — both found in damaged
brain tissue in Alzheimer's.
«The therapy is based on an increase in the levels of this
protein in the
brain using an adeno -
associated viral vector (AAV).
The disease is largely attributed to an abnormal buildup of
proteins, which can form amyloid beta plaques and tangles in the
brain that trigger inflammation and result in the loss of
brain connections called synapses, the effect most strongly
associated with cognitive decline.
«
Protein associated with Parkinson's travels from
brain to gut: New laboratory study provides clues on a particular pathway of «alpha - synuclein» diffusion.»
Elevated levels of these adducts in cord blood were
associated with shorter telomeres — the first time this relationship has been tested — as well as with lower levels of
brain - derived neurotropic factor (BDNF), a
protein involved in neuronal grown.
The overabundance of this
protein leads to the formation of the
brain plaques
associated with Alzheimer's, the researchers believe.
Likewise, certain
brain regions of these optogenetically stimulated, post-stroke mice showed increased levels of
proteins associated with heightened ability of nerve cells to alter their structural features in response to experience — for example, practice and learning.
Researchers know that in the body, the
protein molecules
associated with CAA form plaques that lodge in blood vessel walls in the
brain, but there haven't been detailed examinations of the molecular structure of these plaques until recently.
In addition, other teams at the O'Donnell
Brain Institute are designing tests for the early detection of patients who will develop dementia, and seeking methods to slow or stop the spread of toxic proteins associated with the disease such as beta - amyloid and tau, which are blamed for destroying certain groups of neurons in the b
Brain Institute are designing tests for the early detection of patients who will develop dementia, and seeking methods to slow or stop the spread of toxic
proteins associated with the disease such as beta - amyloid and tau, which are blamed for destroying certain groups of neurons in the
brainbrain.
Thankfully, it has good plumbing: Scientists have just discovered a cleansing river inside the
brain, a fluid stream that might be enlisted to flush away the buildup of
proteins associated with Alzheimer's, Huntington's and other neurodegenerative disorders.
Lewy bodies (accumulation of abnormal alpha - synuclein A
protein in the human
brain that is
associated with the development of Parkinson's.
A
protein in the human
brain that is
associated with the development of Parkinson's.
We will explore whether the intravenous administration of the recombinant
protein is able to reduce Aβ accumulation in the mouse
brain and prevent the cognitive and behavioral deficits
associated with that pathology.
Led by Ed Boyden, an
associate professor of biological engineering and
brain and cognitive sciences at MIT, the researchers described the
protein in the June 29 issue of Nature Neuroscience.
Finally, we generate new tools and mouse models to study the role of de novo
protein synthesis in normal
brain function and in pathophysiology
associated with neurodevelopmental and neurodegenerative disease.
Losing just one night of sleep led to an immediate increase in beta - amyloid, a
protein in the
brain associated with Alzheimer's disease, according to...
The «gold standard» compound for creating neuronal connections is
brain - derived neurotrophic factor, or BDNF, a growth - promoting
protein associated with normal
brain development and learning.
Elevated levels of the
brain protein tau following a sport - related concussion are
associated with a...
This study is important as it shows that a single night of sleep deprivation can lead to an increase in amyloid, a
protein associated with Alzheimer's disease, deposited in the
brain.
The new evidence, published today in Nature Medicine, shows that a reduction of the
protein can severely aggravate symptoms, while increases in progranulin may be the
brain's attempt at fighting the inflammation
associated with the disease.
Maryland, US (Scicasts)-- Losing just one night of sleep led to an immediate increase in beta - amyloid, a
protein in the
brain associated with Alzheimer's disease, according to a small, new study by researchers at the...
and affinity of antibody ACI - 5400 were characterized by a panel of methods: (i) measuring the selectivity for a specific phospho - Tau epitope known to be
associated with tauopathy, (ii) performing a combination of peptide and
protein binding assays, (iii) staining of
brain sections from mouse preclinical tauopathy models and from human subjects representing six different tauopathies, and (iv) evaluating the selective binding to pathological epitopes on extracts from tauopathy
brains in non-denaturing sandwich assays.
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