N-Truncated Abeta Starting with Position Four Early Intraneuronal Accumulation and Rescue of Toxicity Using Nt4x-167, a Novel Monoclonal Antibody

The amyloid hypothesis in Alzheimer disease (AD) considers amyloid beta peptide (Abeta) deposition causative in triggering down-stream events like neurofibrillary tangles, cell loss, vascular damage and memory decline. In the past years N-truncated Abeta peptides especially N-truncated pyroglutamate Abeta pE3-42 have been extensively studied. Together with full-length Abeta 1-42 and Abeta 1-40, N-truncated Abeta pE3-42 and Abeta 4-42 are major variants in AD brain. Although Abeta 4-42 has been known for a much longer time, there is a lack of studies addressing the question whether Abeta pE3-42 or Abeta 4-42 may precede the other in Alzheimer's disease pathology. Abeta 4-x precedes Abeta pE3-x in the well accepted 5XFAD AD mouse model underlining the significance of N-truncated species in AD pathology. NT4X-167 therefore is the first antibody reacting with Abeta 4-x and represents a novel tool in Alzheimer research. Proceeds from the sale of this book go to support an elderly disabled person.