کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2572600 | 1129312 | 2015 | 11 صفحه PDF | دانلود رایگان |
• Synaptic deficits in number and function are at the core of many types of memory disorder.
• Pharmacological agents targeting synaptic functions exhibit universal therapeutic value for many types of memory disorder.
• Treatments targeting the pathophysiology, not the underlying pathology, have high potential.
• Restoring synaptic functions should be considered as one major therapeutic goal in memory therapy.
Evidence is accumulating that many memory disorders, including those due to neurodegenerative diseases, traumatic brain injury (TBI), vascular disease, or abnormal brain development, share common features of memory-related pathology. Structural and functional deficits of synapses are at the core of the underlying pathophysiology, constituting a critical point of convergence in memory disorders. Memory therapeutics that target synaptic loss and dysfunction – that is, to slow, halt, or reverse progression of the disorders at the level of synapses, via synaptogenic molecular cascades such as those of protein kinase C (PKC) and brain-derived neurotrophic factor (BDNF) – possess universal therapeutic value for many forms of memory disorder. They may be useful either as standalone interventions for patients with memory disorders or as adjuncts to drugs that target the underlying pathology.
Journal: - Volume 36, Issue 6, June 2015, Pages 384–394