title: [New therapeutic approaches].
abstract: The most prevalent causes of dementia are progressive and irreversible neurodegenerative diseases of the brain. Alzheimer's disease ranks first and is follwed by Parkinson and Lewy body disease as well as the Frontotemporal lobar degenerations. These neurodegenerative processes are characterised by the production, aggregation and deposition of pathological proteins. These are β amyloid and tau in Alzheimer's disease; α synuclein in der Parkinson's- and Lewy body disease, and tau, TDP-43 as well as FUS in the Frontotemporal lobar degenerations. Aggregation into oligomers and fibrils and subsequent sedimentation of these proteins lead to nerve cell dysfunction, synaptic failure and ultimately to the demise of neurons. The deficits and imbalance of neurotransmitter systems which represent an important target of the current pharmacological treatment of dementia are consequences of nerve cell loss. Many of the novel treatment approaches that are being tested in clinical trials are aimed at preventing, slowing or ameliorating the production, aggregation and deposition of pathological proteins. Key strategies are inhibition of secretases which generate β amyloid, active and passive immunisation against β amyloid, restriction β amyloid and tau aggregation as well as stimulation of β amyloid clearance. In addition clinical trials are ongoing on symptomatic treatments including the simultaneous stimulation of multiple neurotransmitter systems, compensation of brain insulin resistance, and neuroprotection through certain nutrients. In addition to novel drug treatments non-pharmacological interventions are also being developed.
authors: Klinik und Poliklinik für Psychiatrie und Psychotherapie, Klinikum rechts der Isar; Technische Universität München.
authors: Alexander
authors: A
authors: Kurz
authors: Klinik und Poliklinik für Psychiatrie und Psychotherapie, Klinikum rechts der Isar; Technische Universität München.
authors: Timo
authors: T
authors: Grimmer
mesh_terms: D000368:Aged; D000544:Alzheimer Disease / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D053829:Amyloid Precursor Protein Secretases / Q000037:antagonists & inhibitors; D016229:Amyloid beta-Peptides / Q000037:antagonists & inhibitors / Q000276:immunology / Q000378:metabolism; D001921:Brain / Q000187:drug effects* / Q000503:physiopathology; D006801:Humans; D007116:Immunization, Passive; D009419:Nerve Tissue Proteins / Q000187:drug effects / Q000276:immunology; D018377:Neurotransmitter Agents / Q000378:metabolism; D057177:TDP-43 Proteinopathies / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D014611:Vaccination
chemical_list: D016229:Amyloid beta-Peptides; D009419:Nerve Tissue Proteins; D018377:Neurotransmitter Agents; D053829:Amyloid Precursor Protein Secretases