Introduction
In humans and animal models, Alzheimer disease (AD) is characterised by accumulation of amyloid-β peptide (Aβ) and hyperphosphorylated tau protein, neuronal degeneration, and astrocytic gliosis, especially in vulnerable brain regions (hippocampus and cortex).
Primary motor cortex alterations in Alzheimer disease: A study in the 3xTg-AD model
 
  Keywords
 
 
  
   Alzheimer disease
  
 
 
  
   Triple transgenic mouse model
  
 
 
  
   Primary motor cortex
  
 
 
  
   Neuron
  
 
 
  
   Glia
  
 
Introduction
In humans and animal models, Alzheimer disease (AD) is characterised by accumulation of amyloid-β peptide (Aβ) and hyperphosphorylated tau protein, neuronal degeneration, and astrocytic gliosis, especially in vulnerable brain regions (hippocampus and cortex). 
These alterations are associated with <dis>cognitive impairment</dis> (<dis>loss of memory</dis>) and <dis>non-cognitive impairment</dis> (<dis>motor impairment</dis>). 
The purpose of this study was to identify cell changes (neurons and glial cells) and aggregation of Aβ and hyperphosphorylated tau protein in the primary motor cortex (M1) in 3xTg-AD mouse models at an intermediate stage of AD.
Methods
We used female 3xTg-AD mice aged 11 months and compared them to non-transgenic mice of the same age. 
In both groups, we assessed motor performance (open field test) and neuronal damage in M1 using specific markers: BAM10 (extracellular Aβ aggregates), tau 499 (hyperphosphorylated tau protein), GFAP (astrocytes), and Klüver-Barrera staining (neurons).
Results
Female 3xTg-AD mice in intermediate stages of the disease displayed motor and cellular alterations associated with Aβ and hyperphosphorylated tau protein deposition in M1.
Conclusions
Patients with AD display signs and symptoms of <dis>functional impairment</dis> from early stages. 
According to our results, M1 cell damage in intermediate-stage AD affects motor function, which is linked to progression of the disease.
Introduction
In humans and animal models, Alzheimer disease (AD) is characterised by accumulation of amyloid-β peptide (Aβ) and hyperphosphorylated tau protein, neuronal degeneration, and astrocytic gliosis, especially in vulnerable brain regions (hippocampus and cortex). 
These alterations are associated with cognitive impairment (loss of memory) and non-cognitive impairment (motor impairment). 
The purpose of this study was to identify cell changes (neurons and glial cells) and aggregation of Aβ and hyperphosphorylated tau protein in the primary motor cortex (M1) in 3xTg-AD mouse models at an intermediate stage of AD.
Methods
We used female 3xTg-AD mice aged 11 months and compared them to non-transgenic mice of the same age. 
In both groups, we assessed motor performance (open field test) and neuronal damage in M1 using specific markers: BAM10 (extracellular Aβ aggregates), tau 499 (hyperphosphorylated tau protein), GFAP (astrocytes), and Klüver-Barrera staining (neurons).
Results
Female 3xTg-AD mice in intermediate stages of the disease displayed motor and cellular alterations associated with Aβ and hyperphosphorylated tau protein deposition in M1.
Conclusions
Patients with AD display signs and symptoms of functional impairment from early stages. 
According to our results, M1 cell damage in intermediate-stage AD affects motor function, which is linked to progression of the disease.
Introduction
In humans and animal models, Alzheimer disease (AD) is characterised by accumulation of amyloid-β peptide (Aβ) and hyperphosphorylated tau protein, neuronal degeneration, and astrocytic gliosis, especially in vulnerable brain regions (hippocampus and cortex).