Alzheimer’s Disease (AD) is a progressive neurodegenerative disease whose pathology is diagnosed based on the presence of neuritic amyloid beta (Aβ) plaques and neurofibrillary tau (τ) tangles. Because the exact causes of the disease are not clearly understood, there are a number of different mechanisms by which CBP (CREB-binding protein) is hypothesized to play a role in the progression of AD. In many cases of early-onset familial AD (FAD), there are mutations of the proteins that make up the enzyme responsible for the creation of Aβ plaques. CBP activity is decreased in the absence of these proteins (presenilin 1 or presenilin2). Additionally, in mouse models of AD, it has been shown that there is a decrease in neuronal histone acetylation, a critical function of CBP.

• Amidfar M, de Oliveira J, Kucharska E, Budni J, Kim YK (September 2020). “The role of CREB and BDNF in neurobiology and treatment of Alzheimer’s disease”. Life Sciences. 257: 118020. doi:10.1016/j.lfs.2020.118020. PMID 32603820. S2CID 220287306.
• Valor LM, Viosca J, Lopez-Atalaya JP, Barco A (2013-07-31). “Lysine acetyltransferases CBP and p300 as therapeutic targets in cognitive and neurodegenerative disorders”. Current Pharmaceutical Design. 19 (28): 5051–5064. doi:10.2174/13816128113199990382. PMC 3722569. PMID 23448461.