| Literature DB >> 31402121 |
Miao-Kun Sun1, Daniel L Alkon2.
Abstract
Alzheimer's disease (AD), the leading disorder of memory impairment in our aging population, is increasing at an alarming rate. AD is currently identified by three 'gold standard criteria': (i) dementia in life, (ii) amyloid plaques at autopsy, and (iii) neurofibrillary tangles at autopsy. Several autopsy studies have indicated that dementia in life is a consequence of lost synaptic networks in the brain, while many clinical trials targeting neurotoxic amyloid beta (Aβ) have consistently failed to produce therapeutic effects on memory function in AD patients. Restoring cognitive function(s) by activating endogenous repairing/regenerating mechanisms that are synaptogenic and antiapoptotic (preventing neuronal death), however, is emerging as a necessary disease-modifying therapeutic strategy against AD and possibly for other degenerative dementias, such as Parkinson's disease and multi-infarct dementia.Entities:
Keywords: brain-derived neurotrophic factor; bryostatin-1; memory disorders; neurodegeneration; protein kinase C; stem cell
Mesh:
Year: 2019 PMID: 31402121 DOI: 10.1016/j.tips.2019.07.008
Source DB: PubMed Journal: Trends Pharmacol Sci ISSN: 0165-6147 Impact factor: 14.819