What is synaptic loss

Synapses may represent a key nidus for dementia including alzheimer's disease (ad) pathogenesis.Despite this fundamental understanding, there has been little systematic study of synapse loss or the role of synaptic proteins associated with pathology.Researchers have recently learned that the brain is more plastic and moldable.Synaptic loss in multiple system atrophy the safety and scientific validity of this study is the responsibility of the study sponsor and investigators.Part of the difficulty in untangling the data lies in the fact that synaptic dysfunction is inferred from a reduction in either cognitive function itself because that depends upon synaptic connections, or upon 18f‐fdg uptake because synapses consume the majority of energy used by the brain.

Currently, ad is defined by the regional presence of neuritic plaques and neurofibrillary tangles in the brain.Other animal studies confirmed cochlear synaptopathy without loss of hair cells due to aging and noise exposure [3,6,10].Synaptic plasticity is change that occurs at synapses, the junctions between neurons that allow them to communicate.Neurons communicate with one another at junctions called synapses.Abstract the extent and location of neuronal losses necessary or sufficient to produce dementia in patients with alzheimer's disease (ad) is unknown.

The idea that synapses could change, and that this change depended on how active or inactive they were, was first proposed in the 1949 by canadian psychologist donald hebb.Although synaptic loss is thought to be core to the pathophysiology of schizophrenia, the nature, consistency and magnitude of synaptic protein and mrna changes has not been systematically.