A fourth stage of memory consolidation & model mice

Introduction

Alzheimers disease is one of the most well known diseases. We know it affects our memory. However, we still don’t know what part of memory if not all of it.

This page is the first part of a study of the article

Failures to reconsolidate memory in a mouse model of Alzheimer’s disease

by Masuo Ohno

Memory reconsolidation

One of the first signs of Alzheimers disease is the increased difficulty in forming new memories and retaining new information.

This may be caused by a problem in any of the 3 stages of consolidation :

Consolidation

= the process of making a working memory / short term memory into a long term memory

Encoding, storage or retrieval

Retrieval isn’t just about making the information usable, it makes it easier to be changed or to link additional information to it.

After retrieval, the memory that has been destabilised doesn’t disappear. It gets restabilised by the synthesis of proteins.

The destabilisation and restabilisation together are the process of memory reconsolidation.

This process has been found to use different brain regions as the original consolidation proving it as a distinct process.

The relation of Alzheimers disease and this “fourth stage” of consolidation hasn’t been studied as much as the other three which is what this article does.

Alzheimers disease model mice

As their are many difficulties when experimenting with humans, many experiments including this one use animals such as mice to test their ideas.

Mice that have been modified genetically to be as close as possible to human with Alzheimers were used.

These are called Alzheimers disease model mice.

Usually, they have a higher than normal expression of the amyloid precursor protein ( APP ), presenilin ( PS ) and/ or tau genes.

These changes are able to cause

  • Beta Amyloid ( Aß ) deposits
  • neurodefibrillary tangles
  • gliosis and synaptic degeneration
  • memory deficits

Beta amyloid

A protein produced from the amyloid precursor protein (APP)

Some subtypes such as Aβ42 are considered to be neurotoxic

Neurodefibrillary tangle

The abnormal accumulation of the protein tau in neurons

Gliosis

The production of glial cells that normally occurs to repair the brain/ spinal cord after an injury

Like in humans.

Memory was measured by use of contextual far consolidation as it is one of the best ways to evaluate animal memory.

Next Part : Memory of 5xFAD APP/PS1 transgenic mice

Part 3 :Is memory acquisition or reconsolidation the problem in Alzheimers ?

2 Comments

Leave a Comment