Alzheimer’s disease

…PET tracers for Alzheimer's disease and other neurodegenerative proteinopathies, focusing on how neuroinflammation interacts with amyloid, tau and synaptic dysfunction in brain and biofluids. The postdoc works on a multi-tracer in vivo PET study measuring amyloid and tau deposition, astrogliosis and synapse impairment together with cognitive tests, CSF, plasma biomarke

…development for Alzheimer's disease, non-Alzheimer dementias, and other neurodegenerative disorders. Joint programming with the Neural-Immune Interactions meeting connects disease mechanisms and clinical strategy with immune modulation of central nervous system biology.

…Experience in an Alzheimer's Disease Research Center setting, additional molecular and cellular approaches and translational research are valued, as are extramural funding or competitive applications for mentored or independent awards. The total negotiated salary u

…together to share research across Alzheimer’s disease and other dementias. The meeting connects work on mechanisms and diagnosis with risk reduction, prevention, treatment and care. Presentations and discussion provide opportunities to compare emerging findings and research approaches across these areas. The 2027 meeting offers both Chicago and online participation. Abstract submissions are scheduled to open in autumn 2026, and registration in spring 2027. Present

The Institute for Neurodegenerative Diseases at UCSF, in the Sandler Neurosciences Center at Mission Bay, studies how the conformational heterogeneity, maturation and transmission of proteopathic assemblies (prions) of tau, amyloid-beta and alpha-synuclein differ across neural cell types and diseases. The Professional Researcher helps manage and contributes to the Condello Lab's program in ex vivo human molecular neuropathology, biochemistry and advanced optical imaging of postmortem brain from Alzheimer's disease and frontotemporal dementia with tauopathy. Work covers procurement and characte

…protein dysfunction in Alzheimer's disease and related neurodegenerative conditions. The work spans human brain tissue, molecular mechanisms, single-cell analysis, and computational biology in an interdisciplinary team.

…grounding on the SEA-AD Alzheimer's disease atlas, build donor- and brain-region-level representations, and release resulting models, code, data, and research artifacts openly.

The Allen Institute has launched a new moonshot initiative on human brain health and disease called the Brain Health accelerator. This initiative aims to dramatically accelerate our understanding of human brain structure and function, identify the molecular, cellular and circuit basis of disease progression, and pioneer new therapeutic strategies targeting vulnerable and affected cell types. Our mission focuses on taking a human-centric approach to understanding and treating disease, combining a large-scale open science discovery approach across multiple diseases, AI-based disease modeling, an

…human-brain data and characterise Alzheimer’s disease trajectories. Contribute to mechanistic analysis of disease using large-scale molecular, cellular and neuropathology datasets.

Charisse Winston and Alysa Kasen discuss approaches to detecting and understanding Alzheimer’s disease beyond amyloid alone. Winston examines neuronal extracellular vesicles in blood and saliva as potential accessible biomarkers, including their relevance to risk in underrepresented populations. Kasen explores how tau filament structure and post-translational modifications in its surrounding regions influence seeding competence and biological activity. Together the presentations connect molecular and structural mechanisms with earlier detection and the interpretation of tau-related neurodegene

…to spatial deficits in aging and Alzheimer’s disease. Rat sequence-task experiments reveal bidirectional hippocampal–parietal interactions across route-centered, place and egocentric representations. Because that task does not isolate reference-frame use, the laboratory developed a freely available task se

Supports Phase 1–3 trials of combination approaches for Alzheimer’s disease and related dementias, with mechanistic rationale and appropriate biomarkers. Phase 1 support is capped at USD 1 million; Phase 2–3 at USD 2 million over two to three years. Exceptional requests up to USD 3 million require case-by-case consideration. Letters of intent are due 20 October 2026 at 17:00 Eastern time (22 October for ISTAART members); invited full applications follow on 15 December (17 December for members).

Funds experimental advancement of AI-discovered therapeutic leads for Alzheimer’s disease and related dementias. Separate tracks support lead optimization and work enabling an investigational-new-drug submission. Awards are up to USD 1 million over two to three years. Pure algorithm development, general AI platforms, repurposing and clinical trial execution are excluded. Letters of intent are due 20 October 2026 at 17:00 Eastern time (22 October for ISTAART members); invited full applications follow on 15 December (17 December for members).

Bryce Mander presents research on early sleep biomarkers associated with Alzheimer's disease pathophysiology and memory impairment. The William C. Dement Seminar connects sleep and circadian neuroscience with neurodegeneration, cognition and clinically relevant approaches to detecting disease-related change.

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by deficits in episodic memory processing and spatial navigation. Especially, the egocentric neural representation of space, which is important for constructing an egocentric cognitive map, is essential for spatial navigation. However, how spatial navigation deficits relate to egocentric neural representation of space remains unclear. The retrosplenial cortex (RSC) is one of the regions affected by amyloidosis in the early stages of AD and is well known for its role in egocentric spatial representation. Specifically, it cont

…are implicated in neurodegenerative diseases like Alzheimer's disease (AD), where neuronal hyperexcitation has been observed. We present a novel multimodal model that integrates resting-state functional MRI and diffusion-weighted imaging to recapitulate functional and structural connectivity dynamics with high fidelity (citations omitted: double-blind review). This model provides a whole-brain, systems-informed measure of excitation-in

…therapeutic approach for Alzheimer's disease (AD), showing efficacy in improving memory function and physiological biomarkers levels in mice and, in perspective, also human patients. However, its mechanisms of action remain poorly understood. Explanations in terms of boosted neurogenesis or glymphatic clearance have been advanced. Here we probe the alternative hypothesis that this non-invasive and non-pharmacological stimulation acts by increasing the fluidity of brain dynamics. Our hypothesis expands upon prev

Alzheimer's disease (AD) is a progressive neurological disorder characterized by amyloid accumulation and behavioral changes across preclinical and clinical stages. Although AD is currently incurable, emerging machine-learning (ML) approaches are facilitating novel insights into disease etiology and treatment mechanisms. Our study utilized and built upon two open-source ML platforms, DeepLabCut (Mathis et al. 2018) and Variational Animal Motion Encoding (VAME) (Luxem et al. 2022), to track and analyze naturalistic behavior in App knock-in (KI) and 5xFAD transgenic mouse models of AD. New human

…Spatial navigation is disrupted in Alzheimer’s Disease (AD). AD, a neurodegenerative disorder characterised by progressive cognitive decline, is associated with deficits in learning a

Advancing therapies for neurological disorders relies on developing efficient, personalized whole-brain models that can capture mechanistic insights and pathological features. Current challenges in creating such computational models arise from managing a considerable number of adjustable parameters. The conventional manual exploration of this parameter space is a serious limitation for personalizing models to individual subject data [1]. This work aims to address this by approaching the problem as an optimization challenge in the context of developing brain models capable of characterizing in

Alzheimer's disease (AD) is a progressive neurodegenerative condition characterized by extracellular accumulation of amyloid-beta. Estrogen receptors (ERs) are widely recognized as mediators of neuroprotection from various insults. Recent research has highlighted the distinction between nuclear and non-nuclear ER activation mechanisms, positioning non-nuclear ERs as a safer option, devoid of the cardiovascular and cancer risks associated with nuclear ER activation. In this study, we aimed to confirm the neuroprotective potential of PaPE-1, a novel compound that preferentially activates non-nuc

…A-beta plaques in Alzheimer's disease mouse models. We hypothesized that these vascular scars result from non-productive angiogenesis, a process in which total or partial reduction of the DLL4/NOTCH pathway leads to erratic angiogenesis and disassembly of vessels into non-conducting structures1. In this study, our objective was to investigate whether restoring the NOTCH pathway in brain endothelial cells could enhance vessel stability around A-beta plaques. To this aim, we injected the

…to pathophysiology of Alzheimer's disease (AD). The effect of adiponectin (APN), an adipocyte-secreted hormone, on the risk and progression of AD patients remains unclear. APN has been demonstrated to play a protective role in peripheral vasculature, while little is known about its impact on cerebrovascular dysfunction in AD. In this study, we examined the cerebrovascular integrity of wildtype, 5xFAD, APN knockout (APN-/-), and APN-deficient 5xFAD (5xFAD;APN-/-) mice in terms of blood-brain barrier (BBB) permeabil

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the most common cause of dementia. Accumulating experimental evidence shows the important role of tumor necrosis factor-α (TNF-α) signaling in AD, but the exact role of TNF-α in AD is still not completely understood. Although TNF-inhibitors are successfully used for treatment of several autoimmune diseases, like rheumatoid arthritis, total inhibition of TNF-α can cause adverse side effects in neurological diseases. This is attributed to the opposing roles of the two receptors of TNF-α. TNF receptor 1 (TNFR1) predominantly