Fig. 4 The effects of MEXX on escape latencies (a), and swimming distance (b) during the training-trial sessions and on swimming times during the probe-trial session (c) in the Morris water maze task on scopolamine induced memory dysfunction in mice.
Interestingly, memory dysfunction in aged rats, associated with hippocampal retinoid hyposignaling, is alleviated by RA-induced normalization of this retinoid signaling pathway [20].
This suggests that very low amounts of Aβ oligomer could induce memory dysfunction in young mice, or, alternatively, a combination of CCL2 and other inflammatory factors elicited by Aβ production (such as reactive oxygen species) may influence memory formation.
Working memory dysfunction in schizophrenia is a prominent neuropsychological deficit and is considered to be a promising endophenotypic marker to better understand the pathology and risk for the disorder [5], [6], [7].
Together, BACE1+/− gene deletion was able to more specifically improve memory dysfunction in 5XFAD mice; however, the memory benefit produced by partial reduction of BACE1 was observed in an age-related manner and disappeared as disease progressed into the more severe phase in 5XFAD mice.
In fact, the early episodic memory dysfunction in alcoholism may be related to glial cell alteration leading to an insufficient support of neurons; or to axonal damage and demyelination, which can result in an anatomical disconnection of the hippocampus from the main source of its neocortical inputs.
Diabetes accelerates memory dysfunction in a continuous, slowly pathological process.
Synaptic failure is an immediate cause of cognitive decline and memory dysfunction in Alzheimer's disease.
Furthermore, subthreshold scopolamine doses can produce working memory dysfunction in rodents when combined with diazepam [ 24].
Memory dysfunction in type II diabetes mellitus triggers neuronal death and inhibits neurogenesis.
