Background: Blood biomarkers can improve the ability to diagnose dementia, providing new information to better understand the pathophysiology and causes of the disease. Some studies with patients have already shown changes in metabolic profiles among patients with pathological cognitive decline or Alzheimer's disease, when compared to individuals with normal cognition.
Methods: To search for new metabolic biomarkers of dementia, we analyzed serum levels of several metabolites, measured by nuclear magnetic resonance spectroscopy, in elderly individuals, a group with normal cognitive decline (control), and three other groups with cognitive decline. pathological (low, moderate, and severe).
Results: Decreased plasma levels of tyrosine, glutamate, valine, leucine, and isoleucine are associated with worsening of pathological cognitive decline. However, the area under analysis of receptor operating characteristics suggests that tyrosine and glutamate have low specificity and sensitivity. Valine, leucine, and isoleucine are influenced by blood glucose or diabetes, but these conditions do not seem to be of great influence in the differences observed. Isobutyrate, histidine, acetone and unknown-1 metabolite also decrease their plasma levels with increasing CD. Isobutyrate ad histidine could have neuroprotective and antioxidant actions, respectively. To elucidate the role of decreased unknown metabolite-1 as a CD biomarker, it will be necessary to previously investigate its identity. To define and elucidate the role of acetone in pathological CD, additional laboratory and clinical studies must be performed. All these metabolites together may constitute a set of biomarkers with capability to identify pathological CD or dementia.
Significance And Novelty: Decrease of glutamate, tyrosine, valine, leucine, isoleucine, histidine, isobutyrate, acetone and unknown-1 metabolite together are a set of biomarkers able to identify pathological CD or dementia. Histidine, isobutyrate, acetone and unknown-1 metabolite are more specific biomarkers of CD.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.jpba.2023.115815 | DOI Listing |
Trials
January 2025
Department of Neurology, Universitätsmedizin Greifswald, Fleischmannstraße 6, Greifswald, 17489, Germany.
Background: Postoperative delirium (POD) is the most common neurological adverse event among elderly patients undergoing surgery. POD is associated with an increased risk for postoperative complications, long-term cognitive decline, an increase in morbidity and mortality as well as extended hospital stays. Delirium prevention and treatment options are currently limited.
View Article and Find Full Text PDFAlzheimers Res Ther
January 2025
Department of Bioengineering, University of California, San Diego, La Jolla, CA, 92093, USA.
Background: PSEN1, PSEN2, and APP mutations cause Alzheimer's disease (AD) with an early age at onset (AAO) and progressive cognitive decline. PSEN1 mutations are more common and generally have an earlier AAO; however, certain PSEN1 mutations cause a later AAO, similar to those observed in PSEN2 and APP.
Methods: We examined whether common disease endotypes exist across these mutations with a later AAO (~ 55 years) using hiPSC-derived neurons from familial Alzheimer's disease (FAD) patients harboring mutations in PSEN1, PSEN2, and APP and mechanistically characterized by integrating RNA-seq and ATAC-seq.
Sci Rep
January 2025
Department of Neurology, Feinberg School of Medicine, Northwestern University, 303 E. Chicago Ave, Chicago, IL, 60611, USA.
Corticospinal motor neurons (CSMN), located in the motor cortex of the brain, are one of the key components of the motor neuron circuitry. They are in part responsible for the initiation and modulation of voluntary movement, and their degeneration is the hallmark for numerous diseases, such as amyotrophic lateral sclerosis (ALS), hereditary spastic paraplegia, and primary lateral sclerosis. Cortical hyperexcitation followed by in-excitability suggests the early involvement of cortical dysfunction in ALS pathology.
View Article and Find Full Text PDFCell Death Dis
January 2025
Amsterdam UMC location Vrije Universiteit Amsterdam, Department of Molecular Cell Biology and Immunology, De Boelelaan 1117, 1081 HV, Amsterdam, The Netherlands.
Aging of the brain vasculature plays a key role in the development of neurovascular and neurodegenerative diseases, thereby contributing to cognitive impairment. Among other factors, DNA damage strongly promotes cellular aging, however, the role of genomic instability in brain endothelial cells (EC) and its potential effect on brain homeostasis is still largely unclear. We here investigated how endothelial aging impacts blood-brain barrier (BBB) function by using excision repair cross complementation group 1 (ERCC1)-deficient human brain ECs and an EC-specific Ercc1 knock out (EC-KO) mouse model.
View Article and Find Full Text PDFBMJ Case Rep
January 2025
Department of Neurology, Barwon Health, Geelong, Victoria, Australia.
A male in his 20s presented with episodic headache and subsequently developed episodic unilateral weakness, dysphasia and encephalopathy. These paroxysmal episodes persisted over time with the development of background cognitive impairment and neuropsychiatric symptoms. MRI surveillance demonstrated progressive T2 hyperintensity with focal cortical oedema correlating to symptoms observed during clinical episodes.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!