Researchers develop new protocol to study white matter injury in Alzheimer's disease

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Researchers develop new protocol to study white matter injury in Alzheimer's disease
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A new editorial paper was published in Aging (listed by MEDLINE/PubMed as 'Aging (Albany NY)' and 'Aging-US' by Web of Science) Volume 15, Issue 16, entitled, 'Microvascular contributions to white matter injury in Alzheimer's disease.'

Reviewed by Lily Ramsey, LLMSep 13 2023 A new editorial paper was published in Aging " and "Aging-US" by Web of Science) Volume 15, Issue 16, entitled, "Microvascular contributions to white matter injury in Alzheimer's disease."

In their new editorial, researchers Zsolt Bagi, Larry S. Sherman and Stephen A. Back from Augusta University discuss mechanisms of cognitive impairment and dementia. Impairments in the cognitive and executive function of presumed cerebral microvascular origin are important and recently recognized neuropathological manifestations of vascular contributions to cognitive impairment and dementia .

"However, until recently, recognition of the role of WM injury during aging and the progression of Alzheimer's disease and related dementias was very limited." Despite growing interest in VCID and AD/ADRD, there have been few studies of mechanistic links between subcortical small vessel disease, WM injury and cognitive decline. Even though WM constitutes >80% of the human cerebral hemispheres, a PubMed search of AD and WM injury yielded only 381 articles vs. 193,303 articles for AD alone. Notably, 50% of diagnosed AD patients have mixed vascular and AD pathology.

"To provide rigorous access to human WM lesions, we recently developed a unique rapid autopsy brain procurement protocol using specimens donated by participants in the Adult Changes in Thought study, a prospective, population-based study of aging and incident dementia among men and women in Seattle, Washington."Journal reference:Bagi, Z., et al. . Microvascular contributions to white matter injury in Alzheimer’s disease. Aging. doi.org/10.18632/aging.204997.

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