Deans' stroke musings: Imaging study reveals LATE as common, overlapping cause of cognitive decline

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Friday, February 27, 2026

Imaging study reveals LATE as common, overlapping cause of cognitive decline

With your already high risk of dementia post stroke, will your doctor guarantee that this won't occur to you?

With your risk of dementia, you need this prevented.

Parkinson’s Disease May Have Link to Stroke March 2017

1. A documented 33% dementia chance post-stroke from an Australian study? May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`

3. A 20% chance in this research. July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018

The latest here:

Imaging study reveals LATE as common, overlapping cause of cognitive decline

In a retrospective analysis of 944 patients undergoing 18F-fluoro-deoxy-glucose positron emission tomography( [¹⁸F] FDG PET) imaging for cognitive decline, 13% showed imaging patterns consistent with probable limbic-predominant age-related TDP-43 encephalopathy (LATE) -- including 10.6% with mixed LATE and Alzheimer disease (AD) -- while 23.7% were classified as probable AD alone, underscoring LATE as a common and often overlapping contributor to dementia.

Using autopsy-confirmed imaging templates from the Alzheimer’s Disease Neuroimaging Initiative, the study identified distinct regional metabolic and MRI atrophy signatures, particularly involving the medial temporal lobe, entorhinal cortex, and amygdala, and demonstrated synergistic, predominantly left-sided brain involvement in mixed LATE+AD cases, highlighting the growing importance of biomarker-driven differentiation for accurate diagnosis and targeted management in aging populations.

The findings were published in The Journal of Nuclear Medicine.

“The distinction in the causes of these types of dementia is critical, especially in the era of anti-amyloid therapies,” said Satoshi Minoshima, MD, University of Utah, Salt Lake City, Utah. “Because LATE has a different underlying pathology and a seemingly different prognosis, it cannot be diagnosed or treated in the same way as Alzheimer's disease.”

Currently, LATE can only be definitively distinguished from Alzheimer's disease through postmortem neuropathology. Because no clinically approved biomarker is available to identify LATE, physicians rely on a diagnostic framework that focuses on PET, MRI, and clinical assessment.

“This has resulted in a significant gap in the diagnosis and management of LATE,” said Dr. Minoshima. “Our study aimed to introduce a quantitative diagnostic framework using commonly available imaging tests to identify LATE, which can be applied in clinics with limited access to advanced biomarkers.”

The researchers retrospectively analysed 944 patients referred to a tertiary cognitive disorders clinic to investigate biomarkers of probable LATE and AD. Autopsy-confirmed PET templates from the Alzheimer’s Disease Neuroimaging Initiative and University of Utah datasets were used to create 3-dimensional stereotactic surface projection maps, allowing objective classification of patients into probable LATE, probable LATE+AD, and probable AD. MRI volumetry was applied to assess regional brain atrophy.

The study found that 13% of patients exhibited probable LATE (2.4% pure LATE, 10.6% LATE+AD), while 23.7% showed probable AD alone. Pure LATE cases had pronounced medial temporal lobe atrophy, whereas mixed LATE+AD cases showed vulnerability in the orbitofrontal gyrus and lateral temporal lobe. The entorhinal cortex and amygdala were key regions distinguishing mixed from pure pathologies. Notably, LATE+AD cases demonstrated synergistic left-dominant metabolic and structural changes.

“The imaging patterns identified on PET and MRI in this study provide clinicians with a practical tool to detect potential LATE pathology in patients with cognitive impairment and to inform clinical management and future investigations of LATE,” said Dr. Minoshima. “These efforts will ultimately advance precision diagnostics and treatment stratification in molecular imaging and nuclear medicine.”

Reference: https://jnm.snmjournals.org/content/early/2026/01/22/jnumed.125.270614

SOURCE: Society of Nuclear Medicine and Molecular Imaging