Publications by authors named "C A Jongenelen"
Midlife hypertension is an important risk factor for cognitive impairment and dementia, including Alzheimer's disease. We investigated the effects of long-term treatment with two classes of antihypertensive drugs to determine whether diverging mechanisms of blood pressure lowering impact the brain differently. Spontaneously hypertensive rats (SHR) were either left untreated or treated with a calcium channel blocker (amlodipine) or beta blocker (atenolol) until one year of age.
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- Amyloid-beta (Aβ) deposition is a key factor in the development of Alzheimer's disease (AD), but current therapies targeting it have not been successful, highlighting the need for new treatment strategies.
- Transglutaminase-2 (TG2) is associated with AD and modifies protein activity, but its full range of interactions in both healthy and AD-affected brains is not well understood.
- Research using APP23 mouse models and TG2 knockout mice shows that while TG2 absence doesn't significantly impact Aβ pathology, it is linked to changes in networks involved in synaptic transmission and cell adhesion, suggesting a role in the progression of AD.
Absence of tissue transglutaminase reduces amyloid-beta pathology in APP23 mice.
Neuropathol Appl Neurobiol
June 2022
Aims: Alzheimer's disease (AD) is characterised by amyloid-beta (Aβ) aggregates in the brain. Targeting Aβ aggregates is a major approach for AD therapies, although attempts have had little to no success so far. A novel treatment option is to focus on blocking the actual formation of Aβ multimers.
View Article and Find Full Text PDFSelf-interaction, chaperone binding and posttranslational modification of amyloid-beta (Aβ) is essential in the initiation and propagation of Aβ aggregation. Aggregation results in insoluble Aβ deposits characteristic of Alzheimer's disease (AD) brain lesions, i.e.
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- Multiple Sclerosis (MS) is a leading cause of neurological disability in young adults, marked by immune cell infiltration, damage to nerve sheaths, and loss of nerve fibers.
- This study investigates the behavior of specific microglia markers (TMEM119 and P2RY12) in grey and white matter MS lesions to better understand their differentiation and immunological status.
- Findings reveal that white matter lesions have decreased TMEM119 and P2RY12 markers, correlating with lymphocyte activity, while grey matter lesions show no change in these markers, indicating a complex interaction of immune responses in MS pathology.