Saxenda for Alzheimer's disease
liraglutide · Investigational / off-label
Last updated 2026-05-28 15:46 UTCSaxenda (liraglutide) is not FDA-approved for Alzheimer's disease, and any use for this condition is off-label or investigational. Research in animal and cell models suggests liraglutide may reduce plaque load, improve memory, and protect neurons, but human clinical trials are ongoing.
AI summary of the sources below.
| Drug | Saxenda (liraglutide) |
|---|---|
| Condition | Alzheimer's disease |
| Approval status | Investigational / off-label |
| Research papers | 50 |
Saxenda is not FDA-approved for alzheimer's disease; the research below reflects investigational or off-label study only.
Research on liraglutide for alzheimer's disease (50)
- The diabetes drug liraglutide prevents degenerative processes in a mouse model of Alzheimer's disease.
- Drugs developed to treat diabetes, liraglutide and lixisenatide, cross the blood brain barrier and enhance neurogenesis.
- Liraglutide can reverse memory impairment, synaptic loss and reduce plaque load in aged APP/PS1 mice, a model of Alzheimer's disease.
- The diabetes drug liraglutide reverses cognitive impairment in mice and attenuates insulin receptor and synaptic pathology in a non-human primate model of Alzheimer's disease.
- Evaluating the effects of the novel GLP-1 analogue liraglutide in Alzheimer's disease: study protocol for a randomised controlled trial (ELAD study).
- The Neuroprotection of Liraglutide Against Ischaemia-induced Apoptosis through the Activation of the PI3K/AKT and MAPK Pathways.
- The GLP-1 Receptor Agonist Liraglutide Improves Memory Function and Increases Hippocampal CA1 Neuronal Numbers in a Senescence-Accelerated Mouse Model of Alzheimer's Disease.
- The diabetes drug liraglutide ameliorates aberrant insulin receptor localisation and signalling in parallel with decreasing both amyloid-β plaque and glial pathology in a mouse model of Alzheimer's disease.
- Neuroprotective and anti-apoptotic effects of liraglutide on SH-SY5Y cells exposed to methylglyoxal stress.
- Liraglutide protects against amyloid-β protein-induced impairment of spatial learning and memory in rats.
- Liraglutide promotes improvements in objective measures of cognitive dysfunction in individuals with mood disorders: A pilot, open-label study.
- Chronic treatment with the GLP1 analogue liraglutide increases cell proliferation and differentiation into neurons in an AD mouse model.
- Neural correlates of liraglutide effects in persons at risk for Alzheimer's disease.
- Prophylactic liraglutide treatment prevents amyloid plaque deposition, chronic inflammation and memory impairment in APP/PS1 mice.
- The type 2 diabetes drug liraglutide reduces chronic inflammation induced by irradiation in the mouse brain.
- Neuroprotective effects of liraglutide for stroke model of rats.
- Subcutaneous administration of liraglutide ameliorates learning and memory impairment by modulating tau hyperphosphorylation via the glycogen synthase kinase-3β pathway in an amyloid β protein induced alzheimer disease mouse model.
- Liraglutide attenuate central nervous inflammation and demyelination through AMPK and pyroptosis-related NLRP3 pathway.
- Neuroprotective and anti-apoptotic effects of liraglutide in the rat brain following focal cerebral ischemia.
- Liraglutide Alleviates Cognitive Deficit in db/db Mice: Involvement in Oxidative Stress, Iron Overload, and Ferroptosis.
- Liraglutide is neurotrophic and neuroprotective in neuronal cultures and mitigates mild traumatic brain injury in mice.
- Subcutaneous administration of liraglutide ameliorates Alzheimer-associated tau hyperphosphorylation in rats with type 2 diabetes.
- Liraglutide prevents cognitive decline in a rat model of streptozotocin-induced diabetes independently from its peripheral metabolic effects.
- The neuroprotection of liraglutide on Alzheimer-like learning and memory impairment by modulating the hyperphosphorylation of tau and neurofilament proteins and insulin signaling pathways in mice.
- The GLP-1 receptor agonist liraglutide reduces pathology-specific tau phosphorylation and improves motor function in a transgenic hTauP301L mouse model of tauopathy.