The study found lecanemab to be safe and effective in slowing down cognitive decline and clearing brain Aβ deposition in Chinese patients with early AD. The results demonstrate a lower incidence of infusion-related reactions and amyloid-related imaging abnormalities compared to international clinical trials.
A study led by Cold Spring Harbor Laboratory researchers found that inhibiting the protein PTP1B improves learning and memory in an Alzheimer's disease mouse model. This suggests that PTP1B inhibition can also improve microglial function, clearing up Aβ plaques.
Researchers discovered Chlamydia pneumoniae can cause inflammation, nerve cell death and cognitive decline in Alzheimer's disease. The study suggests targeting chronic bacterial infection may represent a new treatment strategy.
A novel viral vector, AAVT42, efficiently delivers therapeutic genes to the brain, restoring memory and protecting neuronal structures in multiple models of Alzheimer's disease. BDNF treatment achieves significant cognitive rescue, facilitating structural repair and suppressing harmful pathways.
Scientists have discovered a new strategy to prevent the formation of toxic tau tangles in brain cells, which are linked to neurodegenerative diseases. By targeting polyserine, an amino acid chain that drives tau misfolding, researchers have found a potential preventative treatment for tauopathies.
Researchers at University College London discovered that Alzheimer's disease disrupts the brain's 'memory replay' process, leading to impaired navigation and memory loss. The study found that even when mice were resting, their brains replayed recent experiences in an altered pattern, which had consequences on memory tasks.
A study published in Cell identified a protein complex called CRL5SOCS4 that marks tau for degradation, suggesting strengthening this natural defense mechanism could represent a new therapeutic strategy. Higher expression of CRL5SOCS4 components made neurons more likely to survive despite the accumulation of tau protein.
The report projects a significant increase in dementia cases across Europe by 2050, with estimated numbers rising to 14.3 million in the EU27 and 19.9 million in EU and non-EU countries combined. Alzheimer Europe urges decision-makers to prioritize dementia research, healthcare infrastructure, and support for families and carers.
A novel AI framework uses speech patterns to detect cognitive decline years before traditional tools can, offering non-invasive screening for neurodegenerative conditions. The approach analyzes complex dynamics and transitions hidden in speech to reveal subtle patterns and extract objective biomarkers from natural patient behavior.
SourcePenn State·JournalFrontiers in Aging Neuroscience·TypeComputational simulation/modeling·DateJan 28, 2026
A new study from Lund University finds that modifiable risk factors like smoking and high blood pressure can damage brain blood vessels and increase dementia risk. Living a healthy lifestyle may help delay symptom onset in Alzheimer's disease.
Researchers developed a new tool to track changes in the synaptic proteome over time, correlating changes to synaptic dysregulation and synapse loss. The results suggest that toxic tau oligomers impact postsynaptic structures first, leading to a dynamic cascade of events that contribute to neurodegeneration.
Researchers at UC San Francisco have identified CUL5, a protein that tags tau for elimination, as a key player in preventing the formation of toxic tau protein clumps that can lead to dementia. The study found that neurons with more CUL5 are less vulnerable to Alzheimer's disease.
A new study led by Dr. Chu Chen suggests that combining THC with celecoxib may improve cognition and reduce Alzheimer's-related brain pathology in mice. The combination produced better outcomes than low-dose THC alone, including improved learning and memory performance and reduced markers of neuroinflammation.
A clinical study will investigate the effects of a three-month at-home intervention with MOVIVE on motor and cognitive responses, utilizing comprehensive assessments and brain imaging techniques. The study aims to inform tailored approaches to assessment and intervention for people with Parkinson's disease.
A new research project aims to develop an eye drop that can detect the fluorescent signal of a protein associated with Alzheimer's disease. If successful, this low-cost and accessible screening tool could help identify patients in their earliest stages of the disease, enabling them to receive early treatment.
The AMALIA project develops a scalable screening platform to identify anti-amyloid therapies, bypassing the challenge of studying amyloid nucleation. This approach enables parallel discovery campaigns on multiple targets, offering unprecedented speed and scalability.
Researchers at UNIGE successfully determined the structure of abnormal protein deposits from a skin biopsy, paving the way for earlier diagnosis and potentially more accessible treatment options. The study's breakthrough opens up new avenues for studying neurodegenerative diseases, including Alzheimer's and Parkinson's.
A multidisciplinary team at USC has developed selective compounds that inhibit an enzyme tied to brain inflammation in people at genetic risk for Alzheimer’s. The inhibitors preserve normal brain function and cross the blood-brain barrier, suggesting a promising therapeutic approach for neurodegenerative diseases.
A study reviews decades of research on Hsp70's role in neurodegenerative diseases, highlighting its protective effects and potential therapeutic value. The review reveals that different Hsp70 isoforms interact with co-chaperones and cellular pathways to determine protein clearance.
Researchers have characterized the association between cellular senescence and human brain structure in both development and late life. The study found that senescence-related gene expression is linked to brain volume and cortical organization, with distinct roles depending on cell type and stage of life.
BrainHealth Week 2026 will explore precision brain health, biosensor technology, and mental resilience, offering actionable strategies for improving daily performance and quality of life. The event brings together industry leaders, scientific community, students, and the community at large to discuss practical roadmap for longevity.
Researchers have discovered that amyloid-β deposits in preeclamptic placentas can disrupt placenta formation, leading to the development of high blood pressure and organ damage. The study found that these deposits impair the ability of placental cells to undergo syncytialization, a critical step in placenta formation.
Researchers found that super agers have a reduced risk of harboring the APOE ε4 gene variant associated with Alzheimer's disease. They also showed a higher frequency of the protective APOE ε2 variant, suggesting a genetic advantage against AD.
Researchers at the University of Virginia Health System have discovered how the keto diet protects against epilepsy seizures by regulating brain cell activity. The team found that a specific cellular receptor, HCAR2, plays a crucial role in reducing seizures, and may be targeted for new treatments.
A new study published in Diabetes, Obesity and Metabolism found that blood sugar spikes after meals may increase the risk of Alzheimer's disease. Individuals with postprandial hyperglycaemia had a 69% greater risk of developing Alzheimer's disease.
ACCESS-AD aims to address Alzheimer's disease challenges with a coordinated framework for diagnosis, treatment and monitoring. The project combines advanced neuroimaging with digital biomarkers to support early patient identification and personalized treatment pathways.
Researchers used single-cell technology to analyze three brain regions of patients with sporadic early onset Alzheimer's disease. They found genes within the entorhinal cortex and hippocampus have severe disruptions consistent with symptomatic involvement in the disease.
Researchers found that close to half of all dementia cases would not arise without the APOE gene's influence, and potentially more than 90% of Alzheimer's disease cases are linked to variants in this single gene. The study highlights the APOE gene as a powerful target for drug development.
A study found that increased bone morphogenetic protein signaling is linked to impaired neurogenesis in Alzheimer's disease, particularly in female mice. The research suggests that activation of BMP signaling may be a key factor contributing to the sex-based differences observed in AD.
A comprehensive review synthesizes emerging evidence on AMPKα isoforms' dual roles in Alzheimer's disease. The analysis proposes that this complexity may explain why pharmacological approaches have yielded mixed results in treating the disease. Isoform-specific targeting is proposed as a novel therapeutic strategy.
Researchers demonstrated that 40-Hz auditory stimulation significantly elevates beta-amyloid levels in the cerebrospinal fluid of aged rhesus monkeys, with effects persisting for over five weeks. The study provides evidence supporting 40-Hz stimulation as a non-invasive therapy for Alzheimer's disease.
Researchers have identified a key protein that produces hydrogen sulfide gas as a therapeutic target for Alzheimer's disease. Experiments in genetically engineered mice show that this protein, Cystathionine γ-lyase (CSE), plays a critical role in cognitive function and memory formation.
Researchers discovered that female brain immune cells called microglia express more interferon-related genes when responding to amyloid-β plaques, causing more harm to neuronal connections. This finding suggests a potential sex-specific treatment approach for Alzheimer's disease.
Researchers discovered that calcium alpha-ketoglutarate restores key memory-related brain functions disrupted in Alzheimer's disease. The molecule enhances synaptic plasticity, protects neurons from degenerative changes, and supports healthier cognitive ageing.
Researchers have successfully reversed Alzheimer's disease in animal models by restoring the brain's energy balance, leading to both pathological and functional recovery. The study used preclinical mouse models and human AD brains to show that maintaining proper NAD+ levels can prevent and even reverse the disease.
Researchers have identified DNA switches that control how brain cells called astrocytes work, which are known to play a role in Alzheimer's disease. The study used CRISPRi technology and single-cell RNA sequencing to test nearly 1000 potential switches, finding that about 150 of them controlled genes implicated in Alzheimer's disease.
In a new study, Northwestern scientists identified a previously unknown toxic sub-species of amyloid beta oligomers that drive brain changes in Alzheimer's disease. NU-9 decreased this toxin and reduced damage in a mouse model, suggesting it could prevent or delay the cascade of toxic events that destroy neurons.
A new study published in Sleep Health found that the quality of a night's sleep, rather than its length, predicts how quickly older adults process information the next day. Researchers analyzed data from 261 participants aged 70 and above, who wore devices to track their sleep and completed cognitive assessments six times a day.
A new study from Mass General Brigham researchers found that hyperphosphorylated tau may help protect the brain from infection, potentially leading to Alzheimer's disease. The study suggests that tau could serve as an antiviral protein against certain viruses.
Scientists at Max Planck Florida Institute for Neuroscience have identified a neural code that allows the brain to track distance traveled without visual cues. This ability is essential for navigation and memory formation, and may offer insight into early navigation problems in Alzheimer's disease.
A new study found that lysophosphatidylcholines (LPCs) promote or protect against Alzheimer's disease depending on a person's genetics. LPCs transport healthy fatty acids to the brain, and their impact is critical in early detection and personalized treatments for those carrying the APOE ε4 gene.
Researchers found that valacyclovir, an antiviral medication, was ineffective in treating early symptomatic Alzheimer's disease and may even worsen cognitive function. The study suggests that individuals with early symptomatic Alzheimer's disease and herpes simplex virus seropositivity should not be treated with valacyclovir.
Scientists at Salk Institute find protein CCN1, secreted by astrocytes, maintains stable neural circuits in adult brains. The discovery could lead to new therapeutics for brain injury and stroke.
A comprehensive review reveals tau protein plays essential roles in brain functions while driving neurodegeneration and psychopathology. Tau deficiency enhances insulin secretion, normalizing glucose levels in diabetic mouse models.
Researchers at UVA Health System discover how traumatic brain injury increases Alzheimer's risk and find a potential prevention strategy using a hollowed-out virus to deliver repair supplies. The approach could help limit neurodegeneration and potentially prevent other neurological diseases.
Researchers summarize advances in multi-target therapies addressing Alzheimer's disease pathology, including Amyloid-beta, tau, neurodegeneration, and cerebrovascular injury. Despite promising preclinical evidence, single-target strategies have shown limited efficacy in clinical trials.
A new study reveals that factors present in aged blood can accelerate the accumulation of amyloid proteins and influence behavior in an experimental mouse model of Alzheimer's. The study found more than 250 differentially expressed proteins linked to synaptic functions, endocannabinoid signaling, and calcium channels.
Researchers developed a new tool, FibrilPaint combined with the FibrilRuler test, to measure the length of toxic Tau amyloid fibrils directly in solution. This 'molecular ruler' represents a major advance in understanding how these fibrils grow, break, and respond to potential drugs.
Researchers at Florida Atlantic University have developed a deep learning model that detects and evaluates Alzheimer's disease (AD) and frontotemporal dementia (FTD) using EEG brainwave analysis. The model achieved over 90% accuracy in distinguishing individuals with dementia from cognitively normal participants.
Researchers will examine protein stability mechanisms in Thermus thermophilus to advance treatments for diseases such as Alzheimer's, ALS, and cancer. The team will explore the structure of Rieske proteins and their role in energy production to understand how to restore stability.
Researchers developed an AI tool to identify patients with undiagnosed Alzheimer's disease using electronic health records, addressing underdiagnosis and healthcare inequities. The model achieved sensitivity rates of 77-81% across diverse populations, promoting fairness while maintaining high accuracy.
Scientists from the Institute of Physical Chemistry discovered a novel molecule, TDMQ20, which can bind to copper ions and decrease its harmful effect on neurons. The researchers found that the complex does not generate reactive oxygen species, making it a promising candidate for treating Alzheimer's disease.
A new dual-action program combines arts sessions for people with dementia with wellbeing sessions for their carers, helping families rediscover connection and confidence. The program was co-designed with those affected by dementia and has been shown to promote social interaction and reduce isolation.
This study found that older mice blood worsens Alzheimer’s-related changes, while younger blood improves memory and cognitive function. The researchers identified key proteins involved in neurodegeneration and inflammation, suggesting new avenues for targeting blood-borne factors to slow or modify disease progression.
UCI MIND is receiving $80 million in new commitments to build a state-of-the-art facility for Alzheimer's disease and related dementias research and patient care. The Quilter family donation has inspired others to pledge support, enabling the institute to advance its critical mission.
Research discovered that eliminating a specific brain protein, Centaurin-α1, can lessen cognitive deficits and brain damage caused by Alzheimer's disease in mice. The study found reduced amyloid plaque formation, improved neuroinflammation, and protected neural connections, suggesting Centaurin-α1 as a potential therapeutic target.
A new study highlights five ways microplastics can trigger inflammation and damage in the brain, including immune cell activity and oxidative stress. Microplastics weaken the blood–brain barrier, causing immune cells to attack them and leading to further damage.
Researchers at USC have identified four distinct layers of specialized cell types in the CA1 region of the mouse hippocampus, a structure vital for memory formation. This discovery changes our understanding of how information is processed in the brain and could explain why certain cells are more vulnerable in diseases like Alzheimer's ...
The EBRAINS Summit 2025 will bring together experts to assess how neuroscience can drive medical progress, digital innovation, and responsible data use. Preliminary results from the EPINOV clinical trial, integrating virtual brain technology for epilepsy surgery planning, will be presented.
A recent study published in Neurology found that people with impaired kidney function have higher levels of Alzheimer's biomarkers in their blood. However, the study did not find an increased risk of developing dementia among those with poor kidney health.