Nerve Loss, Axon Loss but now another problem for the minibrains – Synapse loss


We are a bundle of nerves and when they do not communicate properly symotms occur. The neurons is the head of the nerve the axon is the body and the synapses are the communication points between nerves. The more synapses we have the more connections we can make and that keeps the information superhigh way.

Not we know of the spinal cord and the brain and how they control movement but have you heard about the minibrains of the spinal cord. They help keep you upright and they form your natural gyroscope. So if you are standing there and I push you in the back what to you do?

No you don’t smack/punch me in the mouth…You put your foot forward to stop yourself from falling. You don’t think about it, your minibrain does this and this minibrain connects the ascending (to the brain) and descending (from the brain) nerve pathways and signals them what to do. This communicates across synapses. These are present every where and control inhibition and excitation of nerves. However, that is not the case in MS and we were shocked to see that they had largely disappeared.

See the brown disappearing on the bottom,

The referees didnt believe it, so had to do the same stuff twice..same result

Synaptic loss in the multiple sclerosis spinal cord.Petrova N, Nutma E, Carassiti D, Newman J, Amor S, Altmann DR, Baker D, Schmierer K.Ann Neurol. 2020 Jun 30. doi: 10.1002/ana.25835. Online ahead of print.

Disability in multiple sclerosis (MS) is considered primarily a result of axonal loss. However, correlation with spinal cord cross-sectional area – a predictor of disability – is poor, questioning the unique role of axonal loss. We investigated the degree of synaptic loss in post-mortem spinal cords (18 chronic MS, eight healthy controls) using immunohistochemistry for synaptophysin and synapsin. Substantial (58-96%) loss of synapses throughout the spinal cord was detected, along with moderate (47%) loss of anterior horn neurons, notably in demyelinating MS lesions. We conclude that synaptic loss is significant in chronic MS, likely contributing to disability accrual. 

Synapses are easier to form and protect so may be an ew avenue for treatment and not an mouse in sight

COI the handy work of ProfK

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  • So is this a reason why lesion load doesn’t necessarily correlate with degree of symptoms? And is lesion load a good way of assessing treatment efficacy – or just rely on symptoms?

    • Lesion load is quite good at predicting early into MS, however strength of correlation with disability over time fades away. This is part due to our clinical scales (EDSS) being biased towards ambulation, and standard MRI being insensitive to the pathological substrate (demyelination, remyelination, neuro-axonal/synaptic loss, scaring…). Spinal cord grey matter volume seems to be a reasonable predictor of limb dysfunction, but it’s quite challenging to do this in clinical care, i.e. outside studies. MD mentions PET below, and that’s promising, however diameter of the spinal cord is not much different from your little finger, so resolution is an issue.

  • Could this also relate to mono synaptic reflexes within cord like knee jerk? Or is that different as nerves involved are peripheral and merely synapsing within cord mini-brain?

    Appreciate reflexes usually hyper in MS. Can they also disappear? Mine did and this has always puzzled me.

    • Disappear reflexes can absolutely. Note we also detected significant nerve loss, and if a lesion hits the cord at its entry zone into the cord, reflexes may become weak or absent.

  • Very interesting to see first time these huge progressive spine cord degenerative disease.
    Thanks for learning.



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