title: Drug development in dementia.
abstract: Dementia is a progressive, irreversible decline in cognition that, by definition, impacts on a patient's pre-existing level of functioning. The clinical syndrome of dementia has several aetiologies of which Alzheimer's disease (AD) is the most common. Drug development in AD is based on evolving pathophysiological theory. Disease modifying approaches include the targeting of amyloid processing, aggregation of tau, insulin signalling, neuroinflammation and neurotransmitter dysfunction, with efforts thus far yielding abandoned hopes and ongoing promise. Reflecting its dominance on the pathophysiological stage the amyloid cascade is central to many of the emerging drug therapies. The long preclinical phase of the disease requires robust biomarker means of identifying those at risk if timely intervention is to be possible.
authors.affiliation: Centre for Public Health, Queen's University of Belfast, Block B, Institute of Clinical Sciences, Royal Victoria Hospital, Belfast BT12 6BA, United Kingdom. Electronic address: ecunningham03@qub.ac.uk.
authors.forename: Emma L
authors.initials: EL
authors.lastname: Cunningham
authors.forename: Anthony P
authors.initials: AP
authors.lastname: Passmore
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy* / Q000378:metabolism; D000682:Amyloid / Q000378:metabolism*; D003071:Cognition; D003072:Cognition Disorders / Q000188:drug therapy* / Q000378:metabolism; D003704:Dementia / Q000188:drug therapy / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000188:drug therapy; D007328:Insulin / Q000378:metabolism*; D018377:Neurotransmitter Agents / Q000378:metabolism; D016875:tau Proteins / Q000378:metabolism*
chemical_list: D000682:Amyloid; D007328:Insulin; D018377:Neurotransmitter Agents; D016875:tau Proteins
keywords: API; Alzheimer's disease; Alzheimer's prevention initiative; DIAN; Dementia; Drugs; N-methyl-d-aspartate; NMDA; RNA binding protein; TDP-43; Therapeutic developments; dominantly inherited Alzheimer's network