Are you me? Amyloid-β blocks the conversation between lysosomes and mitochondria.

EMBO J

Clem Jones Centre for Ageing Dementia Research (CJCADR), Queensland Brain Institute (QBI), University of Queensland, Brisbane, QLD, Australia.

Published: November 2018

How amyloid‐β (Aβ) and tau exacerbate Alzheimer's disease (AD) at a subcellular level is only incompletely understood. Norambuena (2018) report crosstalk between mitochondria and lysosomes and identify a role for lysosomal mTORC1 in the nutrient‐induced activation of mitochondria. This lysosomal signalling pathway is strongly inhibited by oligomeric Aβ through the tau‐dependent activation of plasma membrane‐localized mTORC1. Together, these results identify a further role for tau in mediating Aβ toxicity.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6236328PMC
http://dx.doi.org/10.15252/embj.2018100839DOI Listing

Publication Analysis

Top Keywords

identify role
8
me? amyloid-β
4
amyloid-β blocks
4
blocks conversation
4
conversation lysosomes
4
lysosomes mitochondria
4
mitochondria amyloid‐β
4
amyloid‐β aβ
4
aβ tau
4
tau exacerbate
4

Similar Publications

Background: Genetic studies indicate a causal role for microglia, the innate immune cells of the central nervous system (CNS), in Alzheimer's disease (AD). Despite the progress made in identifying genetic risk factors, such as CD33, and underlying molecular changes, there are currently limited treatment options for AD. Based on the immune-inhibitory function of CD33, we hypothesize that inhibition of CD33 activation may reverse microglial suppression and restore their ability to resolve inflammatory processes and mitigate pathogenic amyloid plaques, which may be neuroprotective.

View Article and Find Full Text PDF

Drug Development.

Alzheimers Dement

December 2024

Karolinska Institute, Stockholm, Södermanland and Uppland, Sweden.

Background: Novel anti-amyloid therapies (AAT) for Alzheimer's Disease (AD) have recently been approved in the United States, Japan and China, and are under regulatory review in Europe. Questions remain regarding the long-term effectiveness and value of these drugs when used in routine clinical practice. Data from follow-up studies will be important to inform their optimal use, including criteria for treatment initiation, monitoring strategies, stopping rules, pricing and reimbursement considerations.

View Article and Find Full Text PDF

Drug Development.

Alzheimers Dement

December 2024

Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, Patiala, India.

Background: Neuroinflammation plays an important role in progression of Alzheimer's disease (AD). Interlukin-6 (IL-6) is well identified marker in initiating and regulating inflammation, and formation of senile plaques in brain. Therefore, simultaneous inhibition of both IL-6 and acetylcholinesterase (AChE) may be an effective strategy for AD.

View Article and Find Full Text PDF

Drug Development.

Alzheimers Dement

December 2024

Retromer Therapeutics, New York, NY, USA.

Background: Convergent evidence indicates that deficits in the endosomal recycling pathway underlies pathogenesis of Alzheimer's disease (AD). SORL1 encodes the retromer-associated receptor SORLA that plays an essential role in recycling of AD-associated cargos such as the amyloid precursor protein and the glutamatergic AMPA receptor. Importantly, loss of function pathogenic SORL1 variants are associated with AD.

View Article and Find Full Text PDF

Background: Alzheimer's disease (AD) is the most prevalent cause of dementia accounting for an estimated 60% to 80% of cases. Despite advances in the research field, developing truly effective therapies for AD symptoms remains a major challenge. Sweet almond contain nutrients that have the potential of combating age-related brain dysfunction, by improving learning, memory and neurocognitive performance.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!