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Role of amyloid-β CSF levels in cognitive deficit in MS

Antonietta Gentile1, Francesco Mori2, Sergio Bernardini3

  • 1IRCCS Fondazione Santa Lucia/Centro Europeo per la Ricerca sul Cervello (CERC), 00143 Rome, Italy; Dipartimento di Medicina dei Sistemi, Università Tor Vergata, 00133 Rome, Italy.

Clinica Chimica Acta; International Journal of Clinical Chemistry
|February 10, 2015
PubMed

Insights

Biomarkers like amyloid-beta and synaptic plasticity could help monitor cognitive decline in multiple sclerosis (MS). Combining these measures may improve assessment of cognitive impairment in MS patients.

Area of Science:

  • Neuroscience
  • Neurology

Background:

  • Multiple sclerosis (MS) is a common neurological disease affecting young adults.
  • While traditionally viewed as a white matter (WM) disease, gray matter (GM) is also affected in MS, correlating with cognitive decline.
  • Cognitive deficits are increasingly recognized in early stages of MS, necessitating reliable biomarkers.

Purpose of the Study:

  • To explore the potential of combining amyloid-beta (Aβ) levels and brain synaptic plasticity as biomarkers for cognitive impairment in MS.
  • To review the relevance of Aβ(1-42) and long-term potentiation (LTP) in the context of MS-related cognitive deficits.

Main Methods:

  • Review of existing literature on Aβ(1-42) in cerebrospinal fluid (CSF) and its association with cognitive decline.
  • Discussion of transcranial magnetic stimulation (TMS) as a method to assess brain synaptic plasticity (specifically LTP).

Main Results:

  • Aβ(1-42) levels are associated with cognitive decline, similar to findings in Alzheimer's disease (AD).
  • Brain synaptic plasticity, measurable via TMS, reflects cognitive reserve.
  • Evidence suggests a link between Aβ(1-42) and LTP in the context of MS.

Conclusions:

  • Combined assessment of CSF Aβ(1-42) and synaptic plasticity (LTP) may offer a powerful tool for evaluating cognitive function in MS patients.
  • This combined approach holds promise for monitoring and potentially preventing cognitive impairment in individuals with MS.
Keywords:
Amyloid-βCognitionLong-term potentiationMultiple sclerosisTranscranial magnetic stimulation

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