Although the cerebellum is not among the most renowned brain structures affected in Alzheimer`s disease (AD), recent evidence suggest that it undergoes degenerative changes during the course of the disease. A main neurophysiological feature of AD patients is the remarkable impairment of long term potentiation (LTP)-like cortical plasticity assessed in the primary motor cortex (M1) using theta burst stimulation (TBS) protocols. In healthy conditions, continuous (cTBS) and intermittent TBS (iTBS) of the cerebellum induce respectively long term depression (LTD)-like and LTP-like after effects in the contralateral M1. Here we aimed at examining the effects of cerebellar TBS on contralateral M1 excitability in a sample of 15 AD patients and 12 healthy age matched controls (HS). Motor evoked potentials (MEPs) were obtained in the contralateral M1 before and after cerebellar cTBS and iTBS protocols. As compared to HS, AD patients showed an impairment of LTP-like cortical plasticity mechanisms following cerebellar iTBS. No difference was observed for the cTBS protocol, in which both populations exhibited the expected LTD-like after effect. This study shows that mechanisms of cerebellar-cortical plasticity are impaired in AD. Given its role in high order cognitive functions, new potential therapeutic strategies could be built up in the future to modulate neural activity in the cerebellum in AD.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/s10548-020-00781-6 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
A rare case of adult-onset vanishing white matter leukoencephalopathy with movement disorder, expressing homozygous EIF2B3 and PRKN pathogenic variants.
BMC Neurol
January 2025
Faculty of Medicine, Department of Neurology, Al-Quds University, Jerusalem, Palestine.
Background: Vanishing white matter disease (VWMD) is a rare autosomal recessive leukoencephalopathy. It is typified by a gradual loss of white matter in the brain and spinal cord, which results in impairments in vision and hearing, cerebellar ataxia, muscular weakness, stiffness, seizures, and dysarthria cogitative decline. Many reports involve minors.
View Article and Find Full Text PDFAutosomal-recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) is an early-onset neurodegenerative disease caused by mutations in the SACS gene. The first two mutations were identified in French Canadian populations 20 years ago. The disease is now known as one of the most frequent recessive ataxias worldwide.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Yale School of Medicine, New Haven, CT, USA.
Background: While the apolipoprotein E (APOE) ε4 allele is a well-known risk factor for late-onset Alzheimer's disease (LOAD), not all carriers develop the condition, suggesting the presence of resilience and/or risk factors. The molecular signatures of resilience/risk in the brain, however, have not been thoroughly described, partly due to the scarcity of healthy APOEe4 carriers. This study addresses this gap using a novel multi-tissue, multi-omic dataset from the Religious Order Study and Memory and Aging Project cohorts highly enriched in APOEe4 carriers with and without LOAD.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Brigham and Women's Hospital; Harvard Medical School, Boston, MA, USA.
Background: Anti-amyloid antibodies have been associated with amyloid-related-imaging-abnormalities (ARIA) in AD patients, causing vasogenic edema and microhemorrhages, especially in ApoE4 carriers. Here, we compared recombinant 3D6-L, a murine version of bapineuzumab, and an isotype control IgG2a monoclonal antibody (mAb) to investigate potential mechanisms, including complement activation, involved in these side effects (ARIA-H or microhemorrhages) following passive immunization.
Method: Plaque-rich 16.
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Background: Adenosine receptor 1 (A1R) is the predominant subtype of adenosine receptors, primarily distributed in memory-associated brain regions such as the cortex, hippocampus, and cerebellum. It actively participates in plasticity-regulated synaptic transmission and is crucial for functions related to sleep, arousal, cognition, learning, and memory. In a recent study, we reported that an elevation in A1R signaling mediates aberrant neuron-glial crosstalk in Alzheimer's disease.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!