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Fig. 2 | Molecular Neurodegeneration

Fig. 2

From: Neurotrophic factor small-molecule mimetics mediated neuroregeneration and synaptic repair: emerging therapeutic modality for Alzheimer’s disease

Fig. 2

Aβ plaques and NFTs as hallmarks of AD. AD is characterized by extracellular deposits of Aβ (senile) plaques and intraneuronal NFTs leading to neurodegeneration, and ultimately cognitive impairment and dementia. Aβ plaques are produced by the amyloidogenic processing of APP by β- and γ-secretase enzymes leading to the formation of Aβ peptides (36–43 amino acids) of which the Aβ40 and Aβ42 are the most common. Aβ42 is the most fibrillogenic and thus most amyloidogenic Aβ peptide. Aβ oligomers impair hippocampal LTP, and thus synaptic plasticity, and learning and memory. NFTs are intracellular aggregates of MAP-tau which is abnormally hyperphosphorylated by upregulation of activities of kinases such as GSK3β and Cdk5 or deficit in phosphatases such as PP2A

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