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Mitophagy inhibits amyloid-β and tau pathology and reverses cognitive deficits in models of Alzheimer’s disease
Evidence that mitophagy is impaired in the hippocampus of AD patients, in induced pluripotent stem cell-derived human AD neurons, and in animal AD models is provided, suggesting that impaired removal of defective mitochondria is a pivotal event in AD pathogenesis and thatMitophagy represents a potential therapeutic intervention.
An Iron-responsive Element Type II in the 5′-Untranslated Region of the Alzheimer's Amyloid Precursor Protein Transcript*
Iron regulation of APP mRNA through the APP 5′-UTR points to a role for iron in the metabolism of APP and confirms that this RNA structure can be a target for the selection of small molecule drugs, such as desferrioxamine and clioquinol, which reduce Aβ peptide burden during Alzheimer's disease.
Running-Induced Systemic Cathepsin B Secretion Is Associated with Memory Function.
GLP-1 receptor stimulation preserves primary cortical and dopaminergic neurons in cellular and rodent models of stroke and Parkinsonism
It is demonstrated that Ex-4 can protect neurons against metabolic and oxidative insults, and they provide preclinical support for the therapeutic potential for exendin-4 in the treatment of stroke and PD.
Selective butyrylcholinesterase inhibition elevates brain acetylcholine, augments learning and lowers Alzheimer beta-amyloid peptide in rodent.
- N. Greig, T. Utsuki, D. Lahiri
- Biology, ChemistryProceedings of the National Academy of Sciences…
- 22 November 2005
In rats, cymserine analogs caused long-term inhibition of brain BChE and elevated extracellular ACh levels, without inhibitory effects on acetylcholinesterase, and improved the cognitive performance of aged rats.
Protection and Reversal of Excitotoxic Neuronal Damage by Glucagon-Like Peptide-1 and Exendin-4
- T. Perry, N. Haughey, M. Mattson, J. Egan, N. Greig
- BiologyJournal of Pharmacology and Experimental…
- 1 September 2002
It is reported that GLP-1, and its longer-acting analog exendin-4, can completely protect cultured rat hippocampal neurons against glutamate-induced apoptosis and suggest that such peptides may have potential for halting or reversing neurodegenerative processes in CNS disorders, such as Alzheimer's disease, and in neuropathies associated with type 2 diabetes mellitus.
GLP-1 receptor stimulation reduces amyloid-beta peptide accumulation and cytotoxicity in cellular and animal models of Alzheimer's disease.
Ex-4 ameliorated the diabetic effects of STZ in 3xTg-AD mice, elevating plasma insulin and lowering both plasma glucose and hemoglobin A1c (HbA1c) levels and brain levels of Abeta protein precursor and Abeta were significantly reduced in Ex-4 treated mice.
Glucagon-like peptide-1 decreases endogenous amyloid-beta peptide (Abeta) levels and protects hippocampal neurons from death induced by Abeta and iron.
It is suggested that GLP-1 can modify APP processing and protect against oxidative injury, two actions that suggest a novel therapeutic target for intervention in Alzheimer's disease.
p53 inhibitors preserve dopamine neurons and motor function in experimental parkinsonism
It is reported that two novel synthetic inhibitors of the tumor suppressor protein p53, pifithrin‐α (PFT‐α) and Z‐1‐117, are highly effective in protecting midbrain dopaminergic neurons and improving behavioral outcome in a mouse model of Parkinson's disease.
Cholinesterases: roles in the brain during health and disease.
- C. Ballard, N. Greig, A. Guillozet‐Bongaarts, A. Enz, S. Darvesh
- BiologyCurrent Alzheimer Research
- 30 June 2005
A number of new lines of evidence suggest that both cholinesterase inhibitors (ChEs) may have broader functions in the CNS than previously thought, which relate to both 'classical' esterase activities of the enzymes as well as non-classical actions unrelated to their enzymatic function.