alzheimers-disease
The development of Alzheimer disease (AD) involves a cluster of pathogenic processes, including amyloid-beta (Aβ) deposition, tau-mediated neurodegeneration, chronic neuroinflammation, oxidative stress (OS), metabolic dysregulation, and disruption of circadian rhythms. Nuclear hormone receptor, Retinoic Acid-Related Orphan Receptor Alpha (RORα) was shown to regulate multiple neuroprotective pathw…
The human brain is widely considered to be the most complex object in the universe, making the race to identify, diagnose, and treat neurodegenerative diseases crucial. In the 1990s, Alzheimer’s disease (AD) was diagnosed using cognitive tests and brain imaging, often requiring a post-mortem autopsy for a definitive diagnosis. Treatments focused on managing symptoms rather than targeting the caus…
Nature Neuroscience, Published online: 01 July 2026; doi:10.1038/s41593-026-02356-3 Author Correction: Spinal cord Tau pathology induces tactile deficits and cognitive impairment in Alzheimer’s disease via dysregulation of CCK neurons
Acta Pharmacologica Sinica, Published online: 12 June 2026; doi:10.1038/s41401-026-01808-7 Amyloid-beta fibrils as active contributors to synaptic dysfunction in Alzheimer’s disease
Nature Neuroscience, Published online: 29 May 2026; doi:10.1038/s41593-026-02298-w Disruption of a neuronal-specific protein degradation system, the plasma membrane-bound neuroproteasome, triggers the conversion of endogenous tau into aggregates that mirror those seen in patients with Alzheimer’s disease (AD). Aging and APOE4 — the largest risk factors for AD — induce neuroproteasome loss, which …
Nature Neuroscience, Published online: 29 May 2026; doi:10.1038/s41593-026-02297-x A cellular explanation for how tau aggregates into fibrils in Alzheimer’s disease has been elusive. This paper identifies the failure of ‘neuroproteasomes’ as sufficient to convert tau into paired helical filaments, a process regulated by ApoE and aging.
BackgroundTimely identification of individuals at risk for Alzheimer’s disease (AD) progression remains a major clinical challenge. Traditional cognitive assessments provide limited prognostic insight, while many machine learning (ML) models rely on costly biomarkers or poorly interpretable algorithms that limit clinical scalability. This study evaluated whether widely available baseline demograp…
Nature Communications, Published online: 12 May 2026; doi:10.1038/s41467-026-73075-3 Foldamer M4 inhibits Aβ42 aggregation, disrupts existing assemblies, and restores neuronal function. This foldamer reduces oxidative stress, improves mitochondrial integrity, and alleviates pathology and cognitive decline in an Alzheimer’s disease mouse model.
New research shows that untreated sleep-disordered breathing alters the brain physically. These disruptions may make the brain more vulnerable to Alzheimer’s disease, fundamentally changing how toxic proteins build up across different stages of cognitive decline.

Using a National Institutes of Health grant, the team hopes to identify critical changes in the progression of Alzheimer’s that could lead to earlier, more effective treatments. The post USC researchers to build a new model of neurodegeneration in Alzheimer’s disease appeared first on USC .
White matter (WM) has traditionally been considered structurally important but functionally inert in fMRI research. However, growing evidence indicates that WM exhibits meaningful BOLD fluctuations and participates in functional connectivity. Here, we investigate alterations in WM functional network connectivity (FNC) across the Alzheimer’s disease (AD) spectrum using resting-state fMRI data from…
Research from UC Santa Cruz indicates that the P3 peptide—an alternative cleavage product of the amyloid precursor protein—may play a role in Alzheimer’s disease. For many years, pharmaceutical companies have focused their Alzheimer’s drug development efforts on amyloid beta, a peptide known for forming sticky deposits in the brain. Billions of dollars and decades of [...]
A new study from researchers highlights an unexpected player in Alzheimer’s disease: aging astrocytes. Senescent astrocytes have been identified as a major contributor to Alzheimer’s progression. The cells lose protective functions and fuel inflammation, particularly in APOE4 carriers. The findings highlight senolytic drugs as a potential new therapy. For the first time, the research team [...]
A new class of Alzheimer’s drugs has been shown to slow the condition’s progression by removing clumps of protein known as amyloid plaques from the brain. However, few countries have approved use of the medications as they bring only modest improvements, are expensive and can have serious side effects. Discover more about these controversial drugs and how they have changed our understanding of Al…
After decades of building and revitalizing numerous multimillion-dollar restaurant chains, entrepreneur Ron Shaich is embracing one more challenge: leaving a positive impact on the world. “I’ve had the good fortune to have some success in life,” he says. “I want to make sure I do a good job stewarding the blessings I’ve had and use […]
To better understand the complex genetic and molecular underpinnings of AD in both its sporadic and genetic forms, researchers from the UC Irvine Charlie Dunlop School of Biological Sciences and the UC Irvine School of Medicine conducted groundbreaking research recently published in Nature Genetics.
Brain Awareness Month: An Overview of Alzheimer's Disease Jul 1, 2023 10 min read An Overview of Alzheimer's Disease Authors: Somil Bhushan, Ayush Halder Editor: Raayan Dhar This article was written with the purpose of educating and raising awareness for Alzheimer's Disease for the month of June (Brain Awareness Month) Introduction Alzheimer’s disease is a neurodegenerative disease that primarily…
Li Gan studies how abnormal proteins and the body’s immune system drive Alzheimer’s disease. Read the full story here.

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