Abstract
Key neuropathological hallmarks of Alzheimer's disease (AD) are extracellular amyloid plaques and intracellular accumulation of hyperphosphorylated Tau protein. The mechanisms underlying these neuropathological changes remain unclear. So far, research on AD therapy has had limited success in terms of symptomatic treatments although it has also had several failures for disease-modifying drugs. Gene transfer strategies to the brain have contributed to evaluate in animal models many interesting tracks, some of which should deserve clinical applications in AD patients in the future.
Publication types
-
Research Support, Non-U.S. Gov't
-
Review
MeSH terms
-
Alzheimer Disease / genetics
-
Alzheimer Disease / pathology
-
Alzheimer Disease / therapy*
-
Amyloid Precursor Protein Secretases / administration & dosage
-
Amyloid Precursor Protein Secretases / genetics
-
Animals
-
Antibodies, Neutralizing / therapeutic use
-
Apolipoproteins E / administration & dosage
-
Apolipoproteins E / genetics
-
Aspartic Acid Endopeptidases / administration & dosage
-
Aspartic Acid Endopeptidases / genetics
-
Brain / metabolism
-
Brain / pathology
-
Brain-Derived Neurotrophic Factor / administration & dosage
-
Brain-Derived Neurotrophic Factor / genetics
-
Clinical Trials as Topic
-
Disease Models, Animal
-
Disease Progression
-
Genetic Therapy / methods*
-
Humans
-
Lentivirus / genetics
-
NF-E2-Related Factor 2 / administration & dosage
-
NF-E2-Related Factor 2 / genetics
-
Plaque, Amyloid / genetics
-
Plaque, Amyloid / pathology
-
Plaque, Amyloid / therapy*
-
RNA, Small Interfering / administration & dosage
-
RNA, Small Interfering / genetics
-
Somatomedins / administration & dosage
-
Somatomedins / genetics
Substances
-
Antibodies, Neutralizing
-
Apolipoproteins E
-
Brain-Derived Neurotrophic Factor
-
NF-E2-Related Factor 2
-
NFE2L2 protein, human
-
RNA, Small Interfering
-
Somatomedins
-
Amyloid Precursor Protein Secretases
-
Aspartic Acid Endopeptidases
-
BACE1 protein, human