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What is the spark that lights the fire? Neurodegenerative diseases like Parkinson’s often begin small and then rapidly spread like wildfire. The Halfmann Lab is uncovering the places where…

Before #Parkinsons symptoms appear, changes may already be happening at the molecular level.

In the Halfmann Lab, researchers use #AI to study when proteins first begin to cluster—early signals that could reveal how #neurodegenerative disease begins. #WorldParkinsonsDay

🔗 bit.ly/4vcTpFb

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Neuroimaging findings in neurodegenerative disorders are often complex, as imaging findings in patients with mild signs and symptoms are frequently subtle and ambiguous. In many cases, by the time imaging findings become obvious, patients have already manifested clinically, and the diagnosis is already established or at least highly suspected. 

The radiation-free PCASL-MRI approach helps, based on the perfusion profile, to achieve an early and accurate diagnosis prior to gross morphological alterations when standardized with PET in simultaneous PET-MRI acquisitions. PCASL and PET changes preceded structural atrophy patterns and could aid in establishing early clinical diagnosis. The combination of PET and PCASL boosted the sensitivity of structural MRI and PET by synergistically diagnosing disease conditions. The synergistic effect of PCASL and FDOPA boosted the sensitivity and specificity in classifying disorders with dopaminergic deficit into IPD/APD phenotypes without the need for additional FDG PET or D2-receptor imaging. 

The authors highlight the role of simultaneous PCASL PET-MRI in the workup of complex neurodegenerative conditions with FDG in centers that do not have a cyclotron facility for producing non-FDG tracers. In clear-cut clinical neurodegenerative disorders, where structural changes are equivocal, an additional PCASL sequence can help in early diagnosis without the need for PET studies.

Neuroimaging findings in neurodegenerative disorders are often complex, as imaging findings in patients with mild signs and symptoms are frequently subtle and ambiguous. In many cases, by the time imaging findings become obvious, patients have already manifested clinically, and the diagnosis is already established or at least highly suspected. The radiation-free PCASL-MRI approach helps, based on the perfusion profile, to achieve an early and accurate diagnosis prior to gross morphological alterations when standardized with PET in simultaneous PET-MRI acquisitions. PCASL and PET changes preceded structural atrophy patterns and could aid in establishing early clinical diagnosis. The combination of PET and PCASL boosted the sensitivity of structural MRI and PET by synergistically diagnosing disease conditions. The synergistic effect of PCASL and FDOPA boosted the sensitivity and specificity in classifying disorders with dopaminergic deficit into IPD/APD phenotypes without the need for additional FDG PET or D2-receptor imaging. The authors highlight the role of simultaneous PCASL PET-MRI in the workup of complex neurodegenerative conditions with FDG in centers that do not have a cyclotron facility for producing non-FDG tracers. In clear-cut clinical neurodegenerative disorders, where structural changes are equivocal, an additional PCASL sequence can help in early diagnosis without the need for PET studies.

On #WorldParkinsonsDay, I'd like to highlight “ASL as a Potential Biomarker in Imaging of #Neurodegenerative Disorders” by Prof. Sandhya Mangalore, et al. (Nat. Inst. of Mental Health and Neurosciences, India).

📄 marketing.webassets.siemens-healthineers.com/1a09d90d690b...

#NeuroSky #MRI #PETMRI

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Original post on peterattiamd.com

Research Worth Sharing, April 2026 Edition Paternal exercise shaping offspring fitness via sperm microRNAs, mRNA COVID vaccines enhancing cancer immunotherapy, light-and-sound stimulation as a low-...

#All #exercise #All #risks #Cancer #Cognitive #Health #& […]

[Original post on peterattiamd.com]

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Anti-Tau 4R Antibody (SPC-815) - Rabbit Polyclonal Order Rabbit Anti-Human Tau 4R Polyclonal (SPC-815) from StressMarq. Suitable for WB, DB. High-quality antibodies for scientific research.

New product!💡

StressMarq is pleased to launch an Anti-Tau 4R Antibody (Catalog# SPC-815), optimized for the detection of Tau-4R isoforms, which have been identified as a pathogenic driver in #neurodegenerative diseases.

Learn more🔎 https://bit.ly/4bMeTzP

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Amyotrophic Lateral Sclerosis (ALS): Causes, Symptoms, Diagnosis, Treatment
#ALS #Neurology #Neurodegenerative #MedicalEducation #iPrkashMishra

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Anti-Tau 4R Antibody (SPC-815) - Rabbit Polyclonal Order Rabbit Anti-Human Tau 4R Polyclonal (SPC-815) from StressMarq. Suitable for WB, DB. High-quality antibodies for scientific research.

New product!💡

StressMarq is pleased to launch an Anti-Tau 4R Antibody (Catalog# SPC-815), optimized for the detection of Tau-4R isoforms, which have been identified as a pathogenic driver in #neurodegenerative diseases.

Learn more🔎 https://bit.ly/4bMeTzP

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A graphic announcing that the CIRM Board approves $111M for discovery and clinical research. It details $80 million for six new discovery grants and $31 million for three clinical trial grants, aimed at developing treatments for both rare and common diseases. The CIRM logo is visible at the bottom right.

A graphic announcing that the CIRM Board approves $111M for discovery and clinical research. It details $80 million for six new discovery grants and $31 million for three clinical trial grants, aimed at developing treatments for both rare and common diseases. The CIRM logo is visible at the bottom right.

CIRM's governing board approved over $111 million to support advances in discovery and clinical research for children's #RareDiseases, #VisionLoss, and treatments for #neurodegenerative conditions. Learn more: bit.ly/4dtnLwY

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US Patent 6,630,507  Cannabinoids as Antioxidants and Neuroprotectants
“Cannabinoids have been found to have antioxidant properties, unrelated to NMDA receptor antagonism. This new found property makes cannabinoids useful in the treatment and prophylaxis of wide variety of oxidation associated diseases, such as ischemic, age-related, inflammatory and autoimmune diseases. The cannabinoids are found to have particular application as neuroprotectants, for example in limiting neurological damage following ischemic insults, such as stroke and trauma, or in the treatment of neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease and HIV dementia. Nonpsychoactive cannabinoids, such as cannabidoil, are particularly advantageous to use because they avoid toxicity that is encountered with psychoactive cannabinoids at high doses useful in the method of the present invention. A particular disclosed class of cannabinoids useful as neuroprotective antioxidants is formula (I) wherein the R group is independently selected from the group consisting of H, CH.sub.3, and COCH.sub.3. ##STR1##”

US Patent 6,630,507 Cannabinoids as Antioxidants and Neuroprotectants “Cannabinoids have been found to have antioxidant properties, unrelated to NMDA receptor antagonism. This new found property makes cannabinoids useful in the treatment and prophylaxis of wide variety of oxidation associated diseases, such as ischemic, age-related, inflammatory and autoimmune diseases. The cannabinoids are found to have particular application as neuroprotectants, for example in limiting neurological damage following ischemic insults, such as stroke and trauma, or in the treatment of neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease and HIV dementia. Nonpsychoactive cannabinoids, such as cannabidoil, are particularly advantageous to use because they avoid toxicity that is encountered with psychoactive cannabinoids at high doses useful in the method of the present invention. A particular disclosed class of cannabinoids useful as neuroprotective antioxidants is formula (I) wherein the R group is independently selected from the group consisting of H, CH.sub.3, and COCH.sub.3. ##STR1##”

#Cannabinoids as #Antioxidants and #Neuroprotectants

🌱 #Cannabis +++ The U.S. Patent Office issued #patent6630507 to the U.S. Health and Human Services filed on 2/2/2001. The patent lists the use of certain #cannabinoids found within the #cannabissativaplant […]

[Original post on mastodon.social]

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Description
This application is a 371 of PCT/US99/08769 filed Apr. 21, 1999, which claims benefit of No. 60/082,589 filed Apr. 21, 1998, which claims benefit of No. 60/095,993 filed Aug. 10, 1998.
FIELD OF THE INVENTION
The present invention concerns pharmaceutical compounds and compositions that are useful as tissue protectants, such as neuroprotectants and cardioprotectants. The compounds and compositions may be used, for example, in the treatment of acute ischemic neurological insults or chronic neurodegenerative diseases.

Description This application is a 371 of PCT/US99/08769 filed Apr. 21, 1999, which claims benefit of No. 60/082,589 filed Apr. 21, 1998, which claims benefit of No. 60/095,993 filed Aug. 10, 1998. FIELD OF THE INVENTION The present invention concerns pharmaceutical compounds and compositions that are useful as tissue protectants, such as neuroprotectants and cardioprotectants. The compounds and compositions may be used, for example, in the treatment of acute ischemic neurological insults or chronic neurodegenerative diseases.

🌱 #Cannabis #Hanfwissen #Wissenschaft

Fühlt sich jemand in der Lage über das #Cannabispatent der US-Regierung zu debattieren? Zu erklären was dieses #Patent6630507 medizinisch und politisch bedeutet ❓ 🙏 ❓ ❓

https://patents.google.com/patent/US6630507B1/en […]

[Original post on mastodon.social]

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NIH Awards $2.3M to Maine Scientist to Study Cell’s “Protein Factory”

Thrilled to congratulate Emily Spaulding on this fantastic news—so well deserved!

🧪 👩‍🔬 🧠 #neurodegenerative

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A deep joint-learning proteomics model for diagnosis of six conditions associated with dementia - Nature Medicine ProtAIDe-Dx is a deep joint-learning model that uses plasma proteomics to provide simultaneous probabilistic diagnoses across six conditions associated with aging.

Different #Neurodegenerative conditions can present w/ similar symptoms, making it difficult to distinguish btwn them. Now, researchers Jacob Vogel, Lijun An, et al. have dvlpd an #AI model capable of detecting multiple diseases at once. Learn More in Nature Medicine 👉 www.nature.com/articles/s41...

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Image of 5 smiling people depticting doctors (from left - man wearing blue scrubs, woman in white coat, woman in white coat, man wearing blue scrubs, woman in white coat)

Text reads: March 30 National Doctors Day
Footer reads: bioVie (company logo)

Image of 5 smiling people depticting doctors (from left - man wearing blue scrubs, woman in white coat, woman in white coat, man wearing blue scrubs, woman in white coat) Text reads: March 30 National Doctors Day Footer reads: bioVie (company logo)

To all the physicians conducting research, testing new therapies, treating patients, and providing support for people with #neurological & #neurodegenerative diseases & disorders, on #NationalDoctorsDay, we say THANK YOU.
#Alz #Parkinsons #longCOVID #Medsky 🩵🩺

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Exploring the Origins of Neurodegenerative Diseases Explore the latest scientific research outlining the origins of neurodegenerative diseases, from genetic factors to environmental exposures, aging, and the gut–brain axis.

How much do you know about the origins of #neurodegenerative diseases?

Explore the latest scientific research around genetic factors, environmental exposures, and aging, and what this research means for the future of neurodegenerative diseases.

Read the blog🔬 https://bit.ly/41td1au

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Anti-Tau 4R Antibody (SPC-815) - Rabbit Polyclonal Order Rabbit Anti-Human Tau 4R Polyclonal (SPC-815) from StressMarq. Suitable for WB, DB. High-quality antibodies for scientific research.

New product!💡

StressMarq is pleased to launch an Anti-Tau 4R Antibody (Catalog# SPC-815), optimized for the detection of Tau-4R isoforms, which have been identified as a pathogenic driver in #neurodegenerative diseases.

Learn more🔎 https://bit.ly/4bMeTzP

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Capitainer® SEP10 micro-sampling tech automatically separates #plasma from whole #blood, providing a high-quality & precise sample collection making plasma sampling faster, accessible & highly reliable to advance #biomarkers & #neurodegenerative research

🔗capitainer.com/produ...

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A cell-based reporter of TDP-43 disease states. Top left: In healthy cells, TDP-43 is predominantly nuclear. Within the nucleus, TDP-43 plays important roles in repressing the inclusion of cryptic exons as well as regulating its own transcript levels and isoforms. This ensures appropriate levels of functional TDP-43 within the cell. Top right: In disease, TDP-43 aggregates in the cytoplasm and is lost from the nucleus, leading to both gain-of-function and a loss-of-function. Loss of nuclear function leads to multiple detrimental events. These include DNA damage as well as the inclusion of cryptic exons in transcripts (depicted as orange boxes in the diagram), in turn leading to the production of incorrectly processed transcripts. In addition, disrupted TDP-43 autoregulation leads to unchecked accumulation of the protein’s own transcript. Bottom left: The reporter line developed by Mamede and colleagues enables the study of TDP-43 aggregation in response to stimuli—in this case exposure to TDP-43 protein aggregates that originated from patients with FTD. The reporters are composed of the C-terminal domain of TDP-43 fused to either a green or red fluorescent protein (FRET pairs). When the reporter aggregates, the proximity of TDP-43 FRET pairs enables the quantitative evaluation of aggregation within each cell. Bottom right: Protein aggregates can be quantified after excitation using a blue laser. Cells containing TDP-43 aggregates produce a FRET-positive signal that can be measured using flow cytometry whilst cells that do not have aggregates do not produce a signal. Image created in BioRender.

A cell-based reporter of TDP-43 disease states. Top left: In healthy cells, TDP-43 is predominantly nuclear. Within the nucleus, TDP-43 plays important roles in repressing the inclusion of cryptic exons as well as regulating its own transcript levels and isoforms. This ensures appropriate levels of functional TDP-43 within the cell. Top right: In disease, TDP-43 aggregates in the cytoplasm and is lost from the nucleus, leading to both gain-of-function and a loss-of-function. Loss of nuclear function leads to multiple detrimental events. These include DNA damage as well as the inclusion of cryptic exons in transcripts (depicted as orange boxes in the diagram), in turn leading to the production of incorrectly processed transcripts. In addition, disrupted TDP-43 autoregulation leads to unchecked accumulation of the protein’s own transcript. Bottom left: The reporter line developed by Mamede and colleagues enables the study of TDP-43 aggregation in response to stimuli—in this case exposure to TDP-43 protein aggregates that originated from patients with FTD. The reporters are composed of the C-terminal domain of TDP-43 fused to either a green or red fluorescent protein (FRET pairs). When the reporter aggregates, the proximity of TDP-43 FRET pairs enables the quantitative evaluation of aggregation within each cell. Bottom right: Protein aggregates can be quantified after excitation using a blue laser. Cells containing TDP-43 aggregates produce a FRET-positive signal that can be measured using flow cytometry whilst cells that do not have aggregates do not produce a signal. Image created in BioRender.

In some #neurodegenerative diseases, TDP-43 is both lost from the nucleus & forms clumps in the cytoplasm. These two pathologies can be challenging to model but a study in @plosbiology.org presents a new system that captures both features 🧪 Paper: plos.io/4sxw0g9 Primer: plos.io/4bvWGrw

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A cell-based reporter of TDP-43 disease states. Top left: In healthy cells, TDP-43 is predominantly nuclear. Within the nucleus, TDP-43 plays important roles in repressing the inclusion of cryptic exons as well as regulating its own transcript levels and isoforms. This ensures appropriate levels of functional TDP-43 within the cell. Top right: In disease, TDP-43 aggregates in the cytoplasm and is lost from the nucleus, leading to both gain-of-function and a loss-of-function. Loss of nuclear function leads to multiple detrimental events. These include DNA damage as well as the inclusion of cryptic exons in transcripts (depicted as orange boxes in the diagram), in turn leading to the production of incorrectly processed transcripts. In addition, disrupted TDP-43 autoregulation leads to unchecked accumulation of the protein’s own transcript. Bottom left: The reporter line developed by Mamede and colleagues enables the study of TDP-43 aggregation in response to stimuli—in this case exposure to TDP-43 protein aggregates that originated from patients with FTD. The reporters are composed of the C-terminal domain of TDP-43 fused to either a green or red fluorescent protein (FRET pairs). When the reporter aggregates, the proximity of TDP-43 FRET pairs enables the quantitative evaluation of aggregation within each cell. Bottom right: Protein aggregates can be quantified after excitation using a blue laser. Cells containing TDP-43 aggregates produce a FRET-positive signal that can be measured using flow cytometry whilst cells that do not have aggregates do not produce a signal. Image created in BioRender.

A cell-based reporter of TDP-43 disease states. Top left: In healthy cells, TDP-43 is predominantly nuclear. Within the nucleus, TDP-43 plays important roles in repressing the inclusion of cryptic exons as well as regulating its own transcript levels and isoforms. This ensures appropriate levels of functional TDP-43 within the cell. Top right: In disease, TDP-43 aggregates in the cytoplasm and is lost from the nucleus, leading to both gain-of-function and a loss-of-function. Loss of nuclear function leads to multiple detrimental events. These include DNA damage as well as the inclusion of cryptic exons in transcripts (depicted as orange boxes in the diagram), in turn leading to the production of incorrectly processed transcripts. In addition, disrupted TDP-43 autoregulation leads to unchecked accumulation of the protein’s own transcript. Bottom left: The reporter line developed by Mamede and colleagues enables the study of TDP-43 aggregation in response to stimuli—in this case exposure to TDP-43 protein aggregates that originated from patients with FTD. The reporters are composed of the C-terminal domain of TDP-43 fused to either a green or red fluorescent protein (FRET pairs). When the reporter aggregates, the proximity of TDP-43 FRET pairs enables the quantitative evaluation of aggregation within each cell. Bottom right: Protein aggregates can be quantified after excitation using a blue laser. Cells containing TDP-43 aggregates produce a FRET-positive signal that can be measured using flow cytometry whilst cells that do not have aggregates do not produce a signal. Image created in BioRender.

In some #neurodegenerative diseases, TDP-43 is both lost from the nucleus & forms clumps in the cytoplasm. These two pathologies can be challenging to model but a study in @plosbiology.org presents a new system that captures both features 🧪 Paper: plos.io/4sxw0g9 Primer: plos.io/4bvWGrw

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A cell-based reporter of TDP-43 disease states. Top left: In healthy cells, TDP-43 is predominantly nuclear. Within the nucleus, TDP-43 plays important roles in repressing the inclusion of cryptic exons as well as regulating its own transcript levels and isoforms. This ensures appropriate levels of functional TDP-43 within the cell. Top right: In disease, TDP-43 aggregates in the cytoplasm and is lost from the nucleus, leading to both gain-of-function and a loss-of-function. Loss of nuclear function leads to multiple detrimental events. These include DNA damage as well as the inclusion of cryptic exons in transcripts (depicted as orange boxes in the diagram), in turn leading to the production of incorrectly processed transcripts. In addition, disrupted TDP-43 autoregulation leads to unchecked accumulation of the protein’s own transcript. Bottom left: The reporter line developed by Mamede and colleagues enables the study of TDP-43 aggregation in response to stimuli—in this case exposure to TDP-43 protein aggregates that originated from patients with FTD. The reporters are composed of the C-terminal domain of TDP-43 fused to either a green or red fluorescent protein (FRET pairs). When the reporter aggregates, the proximity of TDP-43 FRET pairs enables the quantitative evaluation of aggregation within each cell. Bottom right: Protein aggregates can be quantified after excitation using a blue laser. Cells containing TDP-43 aggregates produce a FRET-positive signal that can be measured using flow cytometry whilst cells that do not have aggregates do not produce a signal. Image created in BioRender.

A cell-based reporter of TDP-43 disease states. Top left: In healthy cells, TDP-43 is predominantly nuclear. Within the nucleus, TDP-43 plays important roles in repressing the inclusion of cryptic exons as well as regulating its own transcript levels and isoforms. This ensures appropriate levels of functional TDP-43 within the cell. Top right: In disease, TDP-43 aggregates in the cytoplasm and is lost from the nucleus, leading to both gain-of-function and a loss-of-function. Loss of nuclear function leads to multiple detrimental events. These include DNA damage as well as the inclusion of cryptic exons in transcripts (depicted as orange boxes in the diagram), in turn leading to the production of incorrectly processed transcripts. In addition, disrupted TDP-43 autoregulation leads to unchecked accumulation of the protein’s own transcript. Bottom left: The reporter line developed by Mamede and colleagues enables the study of TDP-43 aggregation in response to stimuli—in this case exposure to TDP-43 protein aggregates that originated from patients with FTD. The reporters are composed of the C-terminal domain of TDP-43 fused to either a green or red fluorescent protein (FRET pairs). When the reporter aggregates, the proximity of TDP-43 FRET pairs enables the quantitative evaluation of aggregation within each cell. Bottom right: Protein aggregates can be quantified after excitation using a blue laser. Cells containing TDP-43 aggregates produce a FRET-positive signal that can be measured using flow cytometry whilst cells that do not have aggregates do not produce a signal. Image created in BioRender.

In some #neurodegenerative diseases, TDP-43 is both lost from the nucleus & forms clumps in the cytoplasm. These two pathologies can be challenging to model but a study in @plosbiology.org presents a new system that captures both features 🧪 Paper: plos.io/4sxw0g9 Primer: plos.io/4bvWGrw

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Our Helpline Care Navigator's Cathy and Kaysha had a great day presenting about PSP & CBD and meeting healthcare professionals at the #Neurodegenerative Conditions Awareness event with @inspireneuroc in Farnborough today! #Healthcare #Awareness #neurology

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Our Research Coordinator, Megan Hodgson, is attending the AD/PD International #Conference on Alzheimer’s, Parkinson’s Diseases and related neurological disorders. It focuses on improving treatments for #neurodegenerative conditions.

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15 PhD researchers will develop these technologies to directly address one of neuro's biggest challenges: the extraordinarily high failure rates seen when drugs for #neurodegenerative diseases are developed & tested in experiments on animals that cannot predict human biology.

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Support Research, Education, and Community

Donate Today to Brain Support Network: Every generous gift enables medical research on #neurodegenerative diseases through the brain donations we arrange across the US.

Learn more and donate today: www.brainsupportnetwork.org/donate/

#braindonation

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Future of GLP-1 Medications: New Research, Uses, and Treatment Trends Learn how GLP-1 medications are evolving, from diabetes and weight loss to heart, kidney, and brain health, with insights into new research and trends

The future of #GLP-1 #medications is far more than managing #diabetes or losing #weight. It has been shown in new studies that these medications may also help with #heart #disease. #kidney disease, addiction, and #neurodegenerative diseases. www.mrmed.in/health-libra...

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Neurodegenerative Disease Devices Market Set for Robust Growth Through 2032 Fueled by Neuromodulation Innovations The Neurodegenerative Disease Devices market is expected to grow steadily till 2032, driven by rising demands and innovations in neuromodulation across developed nations.

Neurodegenerative Disease Devices Market Set for Robust Growth Through 2032 Fueled by Neuromodulation Innovations #India #Neuromodulation #Neurodegenerative #Noida #Vyansa

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Label-free in vivo molecular profiling of the human retina by non-resonant Raman spectroscopy - Communications Biology In vivo non-resonant Raman spectroscopy of the optic nerve head enables label-free molecular fingerprinting of the human retina, revealing longitudinal and age-related changes toward early diagnosis o...

👁️Non-invasive method for molecular profiling of the human retina: #Raman #spectroscopy at the optic nerve head reveals age‑linked changes in the retina, establishing its potential as an early diagnostic tool for #ophthalmic and #neurodegenerative disease biomarkers.
www.nature.com/articles/s42...

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Brainstorm Cell Therapeutics Secures Strategic Placement to Fuel Growth in Neurodegenerative Disease Research Brainstorm Cell Therapeutics has successfully raised $2 million through strategic placements, aimed at advancing innovative stem cell therapies for neurodegenerative diseases.

Brainstorm Cell Therapeutics Secures Strategic Placement to Fuel Growth in Neurodegenerative Disease Research #USA #New_York #BrainStorm #stem_cell #Neurodegenerative

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@rpeptide.bsky.social #BetaAmyloid preformed fibrils are the perfect tool and model to assist scientists in the discovery of new treatments & #diagnostictools for #neurodegenerative diseases such as #Alzheimers disease

www.stratech.co.uk/our-partners...

#brainhealth #oligomers #biomarkers

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🎨Science Visuals |🧠Amyotrophic Lateral Sclerosis (#ALS) is a progressive #neurodegenerative disease marked by the loss of upper & lower motor neurons.
🔬Risk factors: genetic mutations (e.g. #SOD1, #C9orf72, #TDP-43) and environmental triggers (e.g. smoking, pesticides, and heavy metals).

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The Innovators Podcast - Joseph Palumbo MD - Chief Medical Officer of BioVie Spotify video

Our CMO, Dr. Joseph Palumbo joined The Innovators Podcast to discuss BioVie’s mission to develop new treatments for #neurological & #neurodegenerative disorders & what it takes to bring a drug from idea to clinic.

Listen here: open.spotify.com/episode/1UZX...

#Parkinsons #LongCOVID #Alz

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Targeting Key Proteins in Fight Against ALS  - News Center Northwestern Medicine scientists have zeroed in on a cellular gatekeeper that may hold promise for treating abnormal protein accumulation in neurodegenerative diseases, according to a study published in Nature Communications. 

Northwestern scientists have identified a cellular gatekeeper that may help treat abnormal protein buildup in #neurodegenerative diseases, per @natcomms.nature.com. spr.ly/63324hov3O

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