Редактирование: NEFM (раздел)

==Publications==

{{medline-entry
|title=Changes in mechanoreceptors in rabbits' anterior cruciate ligaments with age.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30927131
|abstract=At present, a few studies have been done on the changes in the distribution, morphology and quantity of mechanoreceptors in anterior cruciate ligament (ACL) with age. In this study, we observed the changes in mechanoreceptors of healthy rabbits' ACL with age. We found that rabbits' ACLs contained 5 kinds of mechanoreceptors including Ruffini corpuscles, Pacinian corpuscles, Golgitendon bodies, free nerve endings and atypical mechanoreceptors. In each ACL, free nerve endings were the most followed by Ruffini corpuscles, Pacinian corpuscles, Golgitendon bodies and atypical mechanoreceptors in the younger than one-old rabbits. Most of the mechanoreceptors were distributed in the synovium near the attachment points of ACL with the femur and tibia. The total quantity of mechanoreceptors were the most in the 3- and 6-month groups, but did not show a significant difference between the two group (P > 0.05). However, there were significant differences in the total quantity of mechanoreceptors between other groups (all P < 0.05). RT-PCR indicated that [[NEFM]] and [[S100B]] levels increased with age, and reached a peak in the 1-year group with significant differences as compared to other groups. [[NEFM]] and [[S100B]] levels were the second in 6-month and 2-year groups and the lowest in the 1-week group. We can conclude that in rabbits' ACLs, free nerve endings are the most common, followed by Ruffini corpuscles, Pacinian corpuscles and Golgitendon bodies. The total quantity of mechanoreceptors reaches a peak in 3 months, while [[NEFM]] and [[S100B]] reach a peak in 1 year.
|mesh-terms=* Aging
* Animals
* Anterior Cruciate Ligament
* Disease Models, Animal
* Humans
* Mechanoreceptors
* Neurofilament Proteins
* Rabbits
* S100 Calcium Binding Protein beta Subunit
* Tibia
|keywords=* Anterior cruciate ligament
* Knee joint
* Mechanoreceptor
* Proprioception
|full-text-url=https://sci-hub.do/10.1007/s10735-019-09820-4
}}
{{medline-entry
|title=The Alzheimer's disease transcriptome mimics the neuroprotective signature of IGF-1 receptor-deficient neurons.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28595357
|abstract=Seminal studies using post-mortem brains of patients with Alzheimer's disease evidenced aberrant insulin-like growth factor 1 receptor ([[IGF1R]]) signalling. Addressing causality, work in animal models recently demonstrated that long-term suppression of [[IGF1R]] signalling alleviates Alzheimer's disease progression and promotes neuroprotection. However, the underlying mechanisms remain largely elusive. Here, we showed that genetically ablating [[IGF1R]] in neurons of the ageing brain efficiently protects from neuroinflammation, anxiety and memory impairments induced by intracerebroventricular injection of amyloid-β oligomers. In our mutant mice, the suppression of [[IGF1R]] signalling also invariably led to small neuronal soma size, indicative of profound changes in cellular homeodynamics. To gain insight into transcriptional signatures leading to Alzheimer's disease-relevant neuronal defence, we performed genome-wide microarray analysis on laser-dissected hippocampal [[CA1]] after neuronal [[IGF1R]] knockout, in the presence or absence of APP/PS1 transgenes. Functional analysis comparing neurons in early-stage Alzheimer's disease with [[IGF1R]] knockout neurons revealed strongly convergent transcriptomic signatures, notably involving neurite growth, cytoskeleton organization, cellular stress response and neurotransmission. Moreover, in Alzheimer's disease neurons, a high proportion of genes responding to Alzheimer's disease showed a reversed differential expression when [[IGF1R]] was deleted. One of the genes consistently highlighted in genome-wide comparison was the neurofilament medium polypeptide Nefm. We found that [[NEFM]] accumulated in hippocampus in the presence of amyloid pathology, and decreased to control levels under [[IGF1R]] deletion, suggesting that reorganized cytoskeleton likely plays a role in neuroprotection. These findings demonstrated that significant resistance of the brain to amyloid-β can be achieved lifelong by suppressing neuronal [[IGF1R]] and identified IGF-dependent molecular pathways that coordinate an intrinsic program for neuroprotection against proteotoxicity. Our data also indicate that neuronal defences against Alzheimer's disease rely on an endogenous gene expression profile similar to the neuroprotective response activated by genetic disruption of [[IGF1R]] signalling. This study highlights neuronal [[IGF1R]] signalling as a relevant target for developing Alzheimer's disease prevention strategies.
|mesh-terms=* Aging
* Alzheimer Disease
* Amyloid beta-Peptides
* Animals
* Anxiety
* CA1 Region, Hippocampal
* Encephalitis
* Female
* Infusions, Intraventricular
* Male
* Memory Disorders
* Mice
* Mice, Knockout
* Mice, Transgenic
* Neurons
* Neuroprotective Agents
* Receptor, IGF Type 1
* Transcriptome
|keywords=* Alzheimer’s disease
* amyloid-β oligomers
* hippocampus CA1
* insulin-like growth factor receptor
* transcriptome
|full-text-url=https://sci-hub.do/10.1093/brain/awx132
}}