Alzheimer's disease (AD) is a progressive degenerative disease for which there is only minimal treatment is available. Insulin resistance (type 2 diabetes) has been identified as a risk factor for AD. The novel anti diabetic drug, GLP-1 incretin analogue, Liraglutide is now in the market and is being used safely in diabetic patients. It was shown in extensive preclinical studies that liraglutide has a range of properties to protect neurons in mouse models of AD. Liraglutide gets into the brain and decreases microglial activation (brain inflammation) by 50%, reduces amyloid plaque (abnormal protein) formation in the mouse brain, reduces levels of soluble amyloid, normalises brain connectivity, protects the cognitive abilities of mice, prevents progressive neuronal damage as evidenced by maintaining brain glucose metabolism, and finally increases the proliferation of nerve cells and the number of new neurons in the brain. These findings are supported by other published information on the protective properties of GLP-1 analogues. We therefore propose to test the effect of Liraglutide in patients with early Alzheimer's dementia on brain inflammation and brain glucose metabolism using a special type of scan called Positron Emission Tomography (PET). TSPO PET measures the brain inflammation and [18F]FDG PET measures the brain glucose metabolism. Liraglutide can be easily administered through daily subcutaneous injections and does not cause hypoglycaemia in non-diabetic individuals. 62 subjects with a diagnosis of AD will have detailed neurological and neuropsychometric assessment, MRI, TSPO PET and [18F]FDG PET scans at baseline. Subjects will either receive 1.2mg of daily sub cutaneous injection of Liraglutide / placebo for one year with regular assessments. PET and MRI scans will be repeated at the end of one year treatment. We hope to find a reduction in microglial activation along with lower reduction of glucose metabolism over the course of treatment