Two most common causes of dementia in older adults are Alzheimer disease dementia (ADD) and dementia with Lewy bodies (DLB).^1,2 Differentiating between ADD and DLB in the clinical environment remains challenging with high rates of misdiagnosis using the current standard of care.² Up to 50% of neuropathologically confirmed DLB, known as Lewy body disease (LBD), are correctly diagnosed antemortem, with ADD as the most common misdiagnosis.^2,3 Distinguishing DLB from ADD is a vital part of patient care as DLB has a worse prognosis and requires different treatment plans compared with ADD.⁴ Patients with DLB are particularly sensitive to neuroleptics prescribed in dementia care, leading to worsening cognitive and motor functions.⁵ Further, new disease-modifying therapies are approved for ADD, but not for DLB.^6,7

The National Institute on Aging and Alzheimer’s Association developed a research framework for Alzheimer disease (AD) classification using biomarkers such as amyloid, tau, and neurodegeneration.⁸ Amyloid positivity, as assessed using PET or biofluid assays (e.g., AB42/40, ptau217), is a core pathologic, distinguishing feature of AD. However, amyloid and Lewy body copathologies occur in over 50% of patients with LBD and can contribute to diagnostic uncertainty.^2,9,10 In lieu of a DLB biomarker classification framework, current diagnostic criteria recommend combining indicative and supportive biomarkers to improve distinguishing between DLB and ADD. Indicative biomarkers include dopamine transporter scans (DaTscan), myocardial scintigraphy, and polysomnography. Supportive biomarkers are collected using MRI, PET, or SPECT scans, and EEG. Current MRI biomarkers in DLB leverage the relative sparing of the medial temporal lobe (MTL) to aid in differentiation.

Tiny “fires” of inflammation smolder deep within the brain’s memory center, creating a persistent brain fog that makes it harder to think, form new memories or even adapt to new environments, all the while increasing the risk to disorders like Alzheimer’s disease.

Scientists call this slow burn “neuroinflammaging,” and for decades it was thought to be the inevitable price of growing older.

Until now.

A landmark study from researchers at the Texas A&M University Naresh K. Vashisht College of Medicine suggests the inflammatory tide responsible for brain aging and brain fog might actually be reversible. And the solution doesn’t involve brain surgery, but a simple nasal spray.

Led by Dr. Ashok Shetty, university distinguished professor and associate director of the Institute for Regenerative Medicine, along with senior research scientists Dr. Madhu Leelavathi Narayana and Dr. Maheedhar Kodali, the team developed a nasal spray that, with just two doses, dramatically reduced brain inflammation, restored the brain’s cellular power plants and significantly improved memory.

The most surprising part? It all happened within weeks and lasted for months.

The findings, published in the Journal of Extracellular Vesicles, could reshape the future of neurodegenerative therapies and may even change how scientists think about brain aging itself.

Picture this: your brain is a high-performance engine. Over decades, it doesn’t just wear down, it also starts to run hot. Tiny “fires” of inflammation smolder deep within the brain’s memory center, creating a persistent brain fog that makes it harder to think, form new memories or even adapt to new environments, all the while increasing the risk to disorders like Alzheimer’s disease.

Scientists call this slow burn “neuroinflammaging,” and for decades it was thought to be the inevitable price of growing older. Until now.

A landmark study by researchers at Texas A&M University Naresh K. Vashisht College of Medicine suggests the inflammatory tide responsible for brain aging and brain fog might actually be reversible. And the solution doesn’t involve brain surgery, but a simple nasal spray.