The University of Kentucky Sanders-Brown Center on Aging Director Linda Van Eldik, Ph.D., hopes to shed light on how specific brain cells may contribute to the progression of Alzheimer's disease, paving the way for potential new therapeutic approaches.Van Eldik recently received a three-year, $300,000 award from the BrightFocus Foundation to support her research project, "Relationship between astrocyte p38 MAPK, neuroinflammation, and Alzheimer pathology.

Vanavond in ‘De tafel van Gert’: wat als je de diagnose van Alzheimer hebt en de juiste medicatie bestaat maar niet verkrijgbaar is?  Het Nieuwsblad

Title: Could the Flu Shot Help Prevent Alzheimer's?
Category: Health News
Created: 6/29/2022 12:00:00 AM
Last Editorial Review: 6/29/2022 12:00:00 AM

Treatment of Alzheimer's disease using foods, supplements and other natural cures, including alpha lipoic acid.

Provides information on symptoms and warning signs for the various stages of Alzheimer's disease.

Provides information on Alzheimer's disease, including background, causes and risk factors.

Jerry’s Abra Auto Body and Glass, owned by the Kottschade family, has been partnering with the Mankato Moondogs, a summer collegiate baseball team, has partnered with Jerry’s Abra Auto Body and Glass each season since 2017, with the business donating $100 to the Alzheimer’s Association for every home run the team hits. With 38 home […]

The post Jerry’s Abra Auto Body and Glass of Mankato Donates $3,800 to Alzheimer’s Association appeared first on CollisionWeek.

About Alzheimer's disease and how new research may one day offer a cure for the disease.

While growing evidence suggests that there’s a link between blood iron levels and the development of Alzheimer’s disease, new research investigating the effects of an available iron-reducing drug has raised concerns about its use as a treatment for the condition.

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Category: Alzheimer's & Dementia, Brain Health, Body & Mind

Tags: Iron, clinical trials, Alzheimer's disease

Will the United States follow the lead of other countries who have put into law the most radical euthanasia policies?

Alzheimer's disease (AD), a leading cause of dementia and mortality, presents a growing concern due to its irreversible progression and the rising costs of care. Early detection is crucial for managing AD, which begins with memory deterioration caused by the damage to neurons involved in cognitive functions. Although incurable, treatments can manage its symptoms. This study introduces a hybrid AlexNet+ResNet-50 model for AD diagnosis, utilising a pre-trained convolutional neural network (CNN) through transfer learning to analyse MRI scans. This method classifies MRI images into Alzheimer's disease (AD), moderate cognitive impairment (MCI), and normal control (NC), enhancing model efficiency without starting from scratch. Incorporating transfer learning allows for refining the CNN to categorise these conditions accurately. Our previous work also explored atlas-based segmentation combined with a U-Net model for segmentation, further supporting our findings. The hybrid model demonstrates superior performance, achieving 94.21% accuracy in identifying AD cases, indicating its potential as a highly effective tool for early AD diagnosis and contributing to efforts in managing the disease's impact.

For the celebrity or celebrities that have shown genuine and productive support for their chosen charity or charities

The charity had supported almost 100,000 people living with dementia and had a record fundraising year

University of Coimbra Failure by immune cells worsens Alzheimer's disease, reveals study by the University of Coimbra A team from the Center for Neuroscience and Cell Biology (CNC), University of Coimbra (UC) in Portugal discovered how some cells of the immune system lose the ability to fight Alzheimer's disease. This new knowledge can help to find a definitive diagnosis. Ana Luísa Cardoso, the coordinator of the research group, explains that "We found that monocytes (the innate immune system cells) of Alzheimer's patients are unable to move when stimulated by substances produced in the brain, which may lead to reduction of cells that can be recruited to the nervous tissue and participate in fighting the disease."

Source: Dr. Douglas Loe 10/31/2024

Leede Financial analysts Dr. Douglas Loe and Siew Ching Yeo, in a research report published on October 30, 2024, maintained their Speculative Buy rating on ProMIS Neurosciences Inc. (PMN:TSX; PMN:NCM) with a price target of US$9.50. The report follows ProMIS's presentation of interim Phase I data for PMN310, its Alzheimer's disease (AD) candidate, at the Clinical Trials on Alzheimer's Disease (CTAD) conference.

The analysts highlighted the positive safety and pharmacokinetic (PK) data, stating, "We were encouraged (though not overly surprised) to see that the mAb was well-tolerated at all five test doses ranging from 2.5mg/kg-to-40mg/kg." They added, "PK analysis of all of these patient cohorts in this single-ascending dose (SAD) trial suggests that once-monthly dosing may be sufficient to sustain mAb levels both in plasma and in cerebrospinal fluid over time."

Regarding dosing efficacy, the analysts noted, "Importantly, ProMIS indicated in the Jul/24 update that even at 2.5mg/kg dosing, PMN310 levels in CSF were over 100x higher than predicted to be necessary to bind to all beta-amyloid oligomers that could accumulate in CSF in diseased patients."

The analysts emphasized the significance of recent industry developments, particularly AbbVie's acquisition of Aliada Therapeutics, stating, "AbbVie's tangible interest in Phase I-stage AD assets shows us that ProMIS could itself be attractive to future suitors if/when it can document direct impact on cognitive impairment in diseased patients."

The report highlighted ProMIS's financial position following its recent equity offering, noting that the company raised US$30.3M with multiple layers of warrant coverage tied to development milestones.

Leede Financial's valuation methodology combines multiple approaches. The analysts explained, "We are maintaining our Speculative Buy rating and one-year PT of US$9.50 on PMN, with our valuation still based on NPV (30% discount rate) and multiples of our F2029 EBITDA/fd EPS forecasts."

They added, "By direct comparison to Aliada's US$1.4B value, PMN shares would notionally be valued on a fully-diluted basis at US$17.65/shr."

In conclusion, Leede Financial's maintenance of their Speculative Buy rating and US$9.50 price target reflects confidence in ProMIS's development of PMN310 and its potential in the Alzheimer's disease market. The share price at the time of the report of US$1.03 represents a potential return of approximately 822% to the analysts' target price, highlighting the significant upside potential if the company's clinical development plans prove successful.

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Disclosures for Leede Financial Inc., ProMIS Neurosciences Inc., October 30, 2024

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( Companies Mentioned: PMN:TSX; PMN:NCM, )

By 2060, nearly 14 million people in the U.S. will be living with dementia, including Alzheimer’s disease. A new report charts a course for the next 10 years of research in the behavioral and social sciences that can point to possible pathways for slowing or preventing dementia and easing its social and economic impacts.

"Forget about selling products, we're declaring war on Alzheimer's and all neurodegenerative diseases. We're not taking any prisoners." — David Avraham

The award will allow the evaluation of a prototype smart patch in an exploratory clinical study of 50 healthy volunteers

Data-share this, pal: As the man said, you have no obligation to share any of your data and I have no obligation to believe anything you say.

Genetic tests showed that certain patients were predisposed to brain injuries if they took the drugs. That information remained secret.

Alzheimer's patients with high levels of tau and amyloid-beta experience faster cognitive decline.

With powerful tools that sequence the genes that are being expressed in individual cells, scientists have gained new insights into the changes that occur...

With powerful tools that sequence the genes that are being expressed in individual cells, scientists have gained new insights into the changes that occur...

Alzheimer's patients with high levels of tau and amyloid-beta experience faster cognitive decline.

With powerful tools that sequence the genes that are being expressed in individual cells, scientists have gained new insights into the changes that occur...

Alzheimer's patients with high levels of tau and amyloid-beta experience faster cognitive decline.

Cerebrospinal fluid proteomics in patients with Alzheimer’s disease reveals five molecular subtypes with distinct genetic risk profiles  Nature.com

Native-state proteomics of Parvalbumin interneurons identifies unique molecular signatures and vulnerabilities to early Alzheimer’s pathology  Nature.com

Plasma proteomics and lipidomics facilitate elucidation of the link between Alzheimer's disease development and vessel wall fragility  Nature.com

Proteomic changes in Alzheimer’s disease associated with progressive Aβ plaque and tau tangle pathologies  Nature.com

Multiplex cerebrospinal fluid proteomics identifies biomarkers for diagnosis and prediction of Alzheimer’s disease  Nature.com

Serum proteomics reveal APOE-ε4 -dependent and APOE-ε4 -independent protein signatures in Alzheimer’s disease  Nature.com

Hay una serie de moléculas en ensayos clínicos, 16 en fase III, con diferentes mecanismos de acción. Algunas son pequeñas; otras, biológicas y, también existen medicamentos ya aprobados para otro fin que buscan ayudar en la enfermedad neurodegenerativa Leer

Learn what causes aggression for those living with dementia and find gentle ways to comfort your loved one during challenging times.

Diagnosing 'Stage One Alzheimer's Disease' based solely on biomarkers is potentially dangerous to patients.

Cellular oxygen consumption in the brain may shed new light on Alzheimer’s disease onset, progression, and treatment.

¿Cómo debe ser el acompañamiento de los pacientes con Alzheimer?

El Alzheimer, los cuidados conscientes y con amor.

Exercise could be a powerful defense against Alzheimer’s disease. Three dementia researchers explain how it works.

A new drug that slows the pace of Alzheimer's disease is too expensive for too little benefit to be used on the NHS, the watchdog says.

Accumulation of the microtubule-associated protein tau is associated with Alzheimer's disease (AD). In AD brain, tau is abnormally phosphorylated at many sites, and phosphorylation at Ser-262 and Ser-356 plays critical roles in tau accumulation and toxicity. Microtubule affinity–regulating kinase 4 (MARK4) phosphorylates tau at those sites, and a double de novo mutation in the linker region of MARK4, ΔG316E317D, is associated with an elevated risk of AD. However, it remains unclear how this mutation affects phosphorylation, aggregation, and accumulation of tau and tau-induced neurodegeneration. Here, we report that MARK4ΔG316E317D increases the abundance of highly phosphorylated, insoluble tau species and exacerbates neurodegeneration via Ser-262/356–dependent and –independent mechanisms. Using transgenic Drosophila expressing human MARK4 (MARK4wt) or a mutant version of MARK4 (MARK4ΔG316E317D), we found that coexpression of MARK4wt and MARK4ΔG316E317D increased total tau levels and enhanced tau-induced neurodegeneration and that MARK4ΔG316E317D had more potent effects than MARK4wt. Interestingly, the in vitro kinase activities of MARK4wt and MARK4ΔG316E317D were similar. When tau phosphorylation at Ser-262 and Ser-356 was blocked by alanine substitutions, MARK4wt did not promote tau accumulation or exacerbate neurodegeneration, whereas coexpression of MARK4ΔG316E317D did. Both MARK4wt and MARK4ΔG316E317D increased the levels of oligomeric forms of tau; however, only MARK4ΔG316E317D further increased the detergent insolubility of tau in vivo. Together, these findings suggest that MARK4ΔG316E317D increases tau levels and exacerbates tau toxicity via a novel gain-of-function mechanism and that modification in this region of MARK4 may affect disease pathogenesis.

Yueming Hu
Dec 11, 2020; 0:jlr.RA120000919v1-jlr.RA120000919
Research Articles

Apolipoproteins C-I, C-II and C-III interact with ApoE to regulate lipoprotein metabolism and contribute to Alzheimer’s disease pathophysiology. In plasma, apoC-I and C-II exist as truncated isoforms, while apoC-III exhibits multiple glycoforms. This study aimed to 1. delineate apoC-I, C-II and C-III isoform profiles in CSF and plasma in a cohort of non-demented older individuals (n = 61), and 2. examine the effect of APOE4 on these isoforms and their correlation with CSF Aβ42, a surrogate of brain amyloid accumulation. The isoforms of the apoCs were immunoaffinity enriched and measured with MALDI-TOF mass spectrometry, revealing a significantly higher percentage of truncated apoC-I and apoC-II in CSF compared to matched plasma, with positive correlation between CSF and plasma. A greater percentage of monosialylated and disialylated apoC-III isoforms was detected in CSF, accompanied by a lower percentage of the two non-sialylated apoC-III isoforms, with significant linear correlations between CSF and plasma. Furthermore, a greater percentage of truncated apoC-I in CSF, and apoC-II in plasma and CSF, was observed in individuals carrying at least one apoE E4 allele. Increased apoC-I and apoC-II truncations were  associated with lower CSF Aβ42. Finally, monosialylated apoC-III was lower, and disialylated apoC-III greater in the CSF of E4 carriers. Together, these results reveal distinct patterns of the apoCs isoforms in CSF, implying CSF-specific apoCs processing. These patterns were accentuated in APOE E4 allele carriers, suggesting an association between APOE4 genotype and Alzheimer’s disease pathology with apoCs processing and function in the brain.

Oct. 25, 2024 — Aggregation of proteins underlies many human disorders, including Alzheimer’s. Teams from the New Jersey Institute of Technology and Princeton University joined forces to study how the amyloid […]

The post PSC: Anton Simulations Reveal How Alzheimer’s Fibril Growth May Accelerate appeared first on HPCwire.

Holly Oakley
Oct 4, 2006; 26:10129-10140
Neurobiology of Disease

Randy L. Buckner
Aug 24, 2005; 25:7709-7717
Neurobiology of Disease

Holly Oakley
Oct 4, 2006; 26:10129-10140
Neurobiology of Disease