Neurofibrillary degeneration is composed of argentophilic neurofilaments found in the pericaryon of some cortical neurons but is also detected within myelinated axons, dendrites and synapses. Amyloid plaques are formed by aggregation of Aβ peptide. The APP protein can generate the Aβ peptide after proteolysis. Two proteins have been identified as participating in these modifications: Tau protein and Amyloid precursor protein (APP). In Alzheimer’s disease, the modifications identified are amyloid plaques and neurofibrillary degeneration. Lewy neurites can restrain neuronal transport and, thus, compromise neuronal activity and survival. These Lewy neurites pile up in the amygdala and striatum of Parkinsonian patients. Lewy neurites are atypical neurites made up of α-synuclein filaments and granular material. These Lewy bodies are round intraneuronal and positive round inclusions of α-synuclein and ubiquitin. Lewy bodies are existent in the dopaminergic neurons of substantia nigra pars compacta. These are mainly detected in the pigmented neurons of the substantia nigra and in other neuronal populations at the peripheral and central levels. In Parkinson’s disease, insoluble α-synuclein fibrils compose the Lewy bodies and Lewy neurites.
In Parkinson’s and Alzheimer’s disease, protein aggregation concerns α-synuclein, Tau and β-amyloid proteins, respectively, although β-amyloid proteins are equally present in Parkinson’s disease. Protein Aggregation and Dysfunctions of Protein Degradation Systems In the following paragraphs we will detail these mechanisms present in common in these two pathologies. Protein aggregation connected with dysfunctional protein degradation systems, mitochondrial perturbation related with cell death and oxidative stress were identified as mechanisms common to the two most-frequent neurodegenerative diseases in humans : Parkinson’s and Alzheimer’s disease.
Mechanisms Common to Neurodegenerative Diseases: Pakinson's and Alzheimer's disease
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