Year: 2014
Type: article
Abstract: Alzheimer's Disease (AD) is a progressive degenerative disease affecting the central nervous system, characterized by early memory impairments followed by cognitive deficit as aphasia, agnosia and apraxia.AD affects over 35 million individuals worldwide and is expected to affect 115 million by 2050 [1].Cellular and molecular neurodegeneration detected in AD is characterized by synapse and neuronal loss, extracellular amyloid β (Aβ) peptide accumulation and intracellular neurofibrillary tangles (hyperphosphorylated tau) [2,3].Less than 1% of AD cases are familial, (onset before 60 to 65 years of age) due to mutations in three genes, APP, presenilin 1 (PSEN1), and presenilin 2 (PSEN2), all involved in Abeta overproduction [4].To date, high Ab levels were suggested to trigger neuronal dysfunctions as major contributors to disease development in the familial form of AD, but for the majority of AD cases, also called sporadic AD, with no obvious genetic bases, other mechanisms are expected to be responsible.Recently, expression profiles of microRNA (miRNA) in Alzheimer's disease brain revealed alterations in many individual miRNAs, and several in vitro and in vivo studies have suggested that a deregulated microRNA expression could contribute to AD [5,6].
Source: Journal of Cytology & Histology
Author: Christian Barbato
Language: English
Subfield: Cellular and Molecular Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: bronze
Funder: Regione Lazio
OpenAlex ID: W2318723538