Damon Hill (@HillF1):

Just did the L'Etape du Tour. Which is hard. Thanks all who donated. https://t.co/PBXlerlfAN You still can! Its to help us stop Neurological diseases. #Neurological #Disease #medicine #medical #neurologicalmedicine #neurologicaldiseases #f1My Neuro UK FundraiserHelp Damon Hill raise money to support Brain & Spine Foundation

#F1 #F1bot #F1FEN

https://x.com/HillF1/status/1810387286275584054

L'Etape du Tour 2024 For Neuro UK

Help Damon Hill raise money to support Brain & Spine Foundation

JustGiving

Interested in researching #neurogenetics with a supportive environment? We at University of Leicester
have several exciting #PhD projects to study #Evolution, #neurologicaldiseases, #epigenetic, #ageing, #sleep and meal insects biology
Please see details in following link and apply, BOOST welcome!

https://sites.google.com/view/neurogenetics-mibtp/home

Neurogenetics MIBTP projects 2024

Dissecting the interplay of extracellular vesicle signalling and tryptophan metabolism in schizophrenia pathogenesis

Impact of social isolation on grey matter structure and cognitive functions: A population-based longitudinal neuroimaging study

Social isolation contributes to human brain atrophy and cognitive decline, indicating an opportunity to reduce dementia risk by promoting social networks.

#Neuroscience #Brain #Neurology #NeurologicalDiseases #NeurodegenerativeDiseases #Neurodegeneration #Alzheimer
#CognitiveDecline #CognitiveDysfunction #Dementia #Hippocampus #Neuroimaging #NeuroImage #SocialIsolation #SocialBond
#Biomedicine #Health

https://elifesciences.org/articles/83660

Social Bonds Protect Aging Brains

Social isolation can potentially harm brain structure and cognitive performance, suggesting an increased risk of conditions like Alzheimer’s dementia.
A lack of quality social interaction can lead to a decrease in the hippocampus’s volume, crucial for memory formation and retrieval, and poorer cognitive performance.

#Neuroscience #Brain #Neurology #NeurologicalDiseases #NeurodegenerativeDiseases #Neurodegeneration #Alzheimer
#CognitiveDecline #CognitiveDysfunction #Dementia #Hippocampus #Neuroimaging #NeuroImage #SocialIsolation #SocialBond
#Biomedicine #Health

https://neurosciencenews.com/social-aging-neuroscience-brain-23505/

Social Bonds Protect Aging Brains - Neuroscience News

Neuroscience News provides research news for neuroscience, neurology, psychology, AI, brain science, mental health, robotics and cognitive sciences.

Neuroscience News

Astrocyte reactivity influences amyloid-β effects on tau pathology in preclinical Alzheimer’s disease

Aβ was associated with increased plasma phosphorylated tau only in individuals positive for astrocyte reactivity (Ast+).

#Neuroscience #Brain #Neurology #NeurologicalDiseases #NeurodegenerativeDiseases #Neurodegeneration #Neuroinflammation #BetaAmyloid #AmyloidPlaques #Tau #NeurofibrillaryTangles #ReactiveAstrocytes #Astrocytes #Glia #GFAP #Biomarker #Alzheimer #Biomedicine #Health

https://www.nature.com/articles/s41591-023-02380-x

Astrocyte reactivity influences amyloid-β effects on tau pathology in preclinical Alzheimer’s disease - Nature Medicine

Cross-sectional and longitudinal analyses of tau pathology in preclinical Alzheimer’s disease reveal that tau tangles accumulate as a function of amyloid-β burden only in individuals positive for an astrocyte reactivity biomarker.

Nature
Functional roles of reactive astrocytes in neuroinflammation and neurodegeneration - Nature Reviews Neurology

Astrocytes are essential for neuronal survival and function in the CNS but, under pathological conditions, they can adopt potentially harmful reactive states. This Review highlights how ‘omics’ technologies can enable the functional characterization of defined reactive astrocyte states in various pathological scenarios.

Nature
Therapeutic Strategies for Spinocerebellar Ataxia Type 1

Spinocerebellar ataxia type 1 (SCA1) is an autosomal dominant neurodegenerative disorder that affects one or two individuals per 100,000. The disease is caused by an extended CAG repeat in exon 8 of the ATXN1 gene and is characterized mostly by a profound loss of cerebellar Purkinje cells, leading to disturbances in coordination, balance, and gait. At present, no curative treatment is available for SCA1. However, increasing knowledge on the cellular and molecular mechanisms of SCA1 has led the way towards several therapeutic strategies that can potentially slow disease progression. SCA1 therapeutics can be classified as genetic, pharmacological, and cell replacement therapies. These different therapeutic strategies target either the (mutant) ATXN1 RNA or the ataxin-1 protein, pathways that play an important role in downstream SCA1 disease mechanisms or which help restore cells that are lost due to SCA1 pathology. In this review, we will provide a summary of the different therapeutic strategies that are currently being investigated for SCA1.

MDPI

APOE expression and secretion are modulated by mitochondrial dysfunction

This study presents compelling evidence that ApoE is upregulated in various models of mitochondrial respiratory chain dysfunction. The work is of fundamental interest for those studying neurodegeneration and the role of ApoE in Alzheimer's disease; future work will be needed to reveal the molecular basis of this dramatic phenotype.

#Biomedicine #Neuroscience #Brain #Neurology #NeurologicalDiseases #NeurodegenerativeDiseases #Neurodegeneration #Alzheimer #ApoE #Neurogenetics #Mitochondria #MitochondrialDysfunction

https://elifesciences.org/articles/85779