Abstract: In various embodiments compounds that induce and/or promote autophagy are provided as wells as methods of use thereof (e.g., in the prophylaxis or treatment of chronic pathologies associated with aging). In one illustrative, but non-limiting embodiments the compound(s) comprise, inter alia, coumarin 106.

Abstract: This invention establishes a new paradigm for treatment of Parkinson's disease (PD) by eliminating senescent cells that reside in or around the site of the disease pathophysiology. Exposure of test subjects to the herbicide paraquat (PQ) increases the risk for developing Parkinson's disease. The data in this disclosure show that PQ induces a senescence arrest and SASP in astrocytes, in culture and in vivo in mice, and senescent cell markers were present in astrocytes in midbrain tissue from PD patients. In a transgenic mouse model, senescent cell ablation protected against PQ-induced PD-like neuropathology. Removal of senescent cells from affected sites using small molecule agents that specifically target senescent cells can help prevent or ameliorate signs and symptoms of the disease.

Abstract: This invention establishes a new paradigm for treatment of Parkinson's disease (PD) by eliminating senescent cells that reside in or around the site of the disease pathophysiology. Exposure of test subjects to the herbicide paraquat (PQ) increases the risk for developing Parkinson's disease. The data in this disclosure show that PQ induces a senescence arrest and SASP in astrocytes, in culture and in vivo in mice, and senescent cell markers were present in astrocytes in midbrain tissue from PD patients. In a transgenic mouse model, senescent cell ablation protected against PQ-induced PD-like neuropathology. Removal of senescent cells from affected sites using small molecule agents that specifically target senescent cells can help prevent or ameliorate signs and symptoms of the disease.

Abstract: In various embodiments methods of delaying the onset of and/or mitigating the severity of one or more symptoms of Parkinson's disease in a mammal are provided. In certain embodiments the methods involve administering to a mammal diagnosed as having or as at risk for Parkinson's disease a chronic low dose of lithium (e.g., a subtherapeutic dose). In certain embodiments the low dose lithium is administered in conjunction with another agent (e.g., L-DOPA).

Abstract: This invention pertains to the discovery that elevated level of free iron causal in the onset and/or progression of diseases characterized by neural degeneration (e.g., Parkinson's Disease). It was also discovered that lowering free iron levels can inhibit (e.g. reduce or eliminate) the onset and/or progression of one or more symptoms of such diseases. Thus, in one embodiment this invention provides a method of inhibiting neural degeneration in a mammal. The method involves reducing free iron levels in a neural tissue of said animal in an amount sufficient to inhibit neural degeneration in said neural tissue.