The results of the present study show that DLPhtEtn ameliorates age-related spatial memory decline without affecting motor activities or fear memory, possibly by protecting hippocampal neuronal death.
Dementia is an umbrella term describing a collection of diseases characterised by progressive neurological decline affecting language, memory, perception, personality and cognitive skills.
The unstoppable death of brain cells in Huntington's leaves patients in permanent decline, affecting their movement, behaviour, memory and ability to think clearly.
Given the essential role of temporomesial structures in declarative long-term memory formation, surgical treatment for mTLE is primarily associated with a risk of material-specific memory decline, but other cognitive domains may be affected as well.
However, these impairments are not the result of massive cell death, indicating that more subtle mechanisms must be affected by aging to produce memory decline.
However, these impairments are not paralleled by an increase in neuronal death (Burke & Barnes, 2006), indicative that more subtle mechanisms must be affected by aging to produce memory decline.
In this context, poor memory may affect decision quality, particularly in individuals with memory decline, such as older adults.
INTRODUCTION Family history (FH) of Alzheimer's disease (AD) affects mitochondrial function and may modulate effects of translocase of the outer mitochondrial membrane 40 kDa (TOMM40) rs10524523 ('523) poly-T length on memory decline.
Episodic memory and working memory decline with advancing age.
Patients who underwent TL demonstrated material-specific memory decline in retrograde memory.
