Properties of NACP/α-synuclein and its role in Alzheimer’s disease
The precursor of the non-amyloid β/A4 protein (non-Aβ) component of Alzheimer’s disease amyloid (NACP)/α-synuclein is the human homologue of α-synuclein, a member of a protein family which includes α-, β- and γ-synuclein. This protein is thought to be involved in neuronal plasticity because of its u...
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| Published in | BBA - Molecular Basis of Disease Vol. 1502; no. 1; pp. 95 - 109 |
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| Main Author | |
| Format | Book Review Journal Article |
| Language | English |
| Published |
Netherlands
Elsevier B.V
26.07.2000
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| Abstract | The precursor of the non-amyloid β/A4 protein (non-Aβ) component of Alzheimer’s disease amyloid (NACP)/α-synuclein is the human homologue of α-synuclein, a member of a protein family which includes α-, β- and γ-synuclein. This protein is thought to be involved in neuronal plasticity because of its unique expression, mainly in the telencephalon during maturation. Consequently, disarrangement of NACP/α-synuclein might disrupt synaptic activity, resulting in memory disturbance. Previous studies have shown that damage to synaptic terminals is closely associated with global cognitive impairment and is an early event in the pathogenesis of Alzheimer’s disease. Although the relationship between synaptic damage and amyloidogenesis is not clear, some proteins at the synaptic site have been implicated in both neuronal alteration and amyloid formation. Indeed, abnormal accumulation of both NACP/α-synuclein and Aβ precursor protein occurs at synapses of Alzheimer’s patients. Other evidence suggests that NACP/α-synuclein is a component of the Lewy bodies found in patients with Parkinson’s disease or dementia with Lewy bodies, and that a point mutation in this protein may be the cause of familial Parkinson’s disease. Consequently, abnormal transport, metabolism or function of NACP/α-synuclein appears to impair synaptic function, which induces, at least in part, neuronal degeneration in several neurodegenerative diseases. |
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| AbstractList | The precursor of the non-amyloid beta /A4 protein (non-A beta ) component of Alzheimer's disease amyloid (NACP)/ alpha -synuclein is the human homologue of alpha -synuclein, a member of a protein family which includes alpha -, beta - and gamma -synuclein. This protein is thought to be involved in neuronal plasticity because of its unique expression, mainly in the telencephalon during maturation. Consequently, disarrangement of NACP/ alpha -synuclein might disrupt synaptic activity, resulting in memory disturbance. Previous studies have shown that damage to synaptic terminals is closely associated with global cognitive impairment and is an early event in the pathogenesis of Alzheimer's disease. Although the relationship between synaptic damage and amyloidogenesis is not clear, some proteins at the synaptic site have been implicated in both neuronal alteration and amyloid formation. Indeed, abnormal accumulation of both NACP/ alpha -synuclein and A beta precursor protein occurs at synapses of Alzheimer's patients. Other evidence suggests that NACP/ alpha -synuclein is a component of the Lewy bodies found in patients with Parkinson's disease or dementia with Lewy bodies, and that a point mutation in this protein may be the cause of familial Parkinson's disease. Consequently, abnormal transport, metabolism or function of NACP/ alpha -synuclein appears to impair synaptic function, which induces, at least in part, neuronal degeneration in several neurodegenerative diseases. The precursor of the non-amyloid beta/A4 protein (non-Abeta) component of Alzheimer's disease amyloid (NACP)/alpha-synuclein is the human homologue of alpha-synuclein, a member of a protein family which includes alpha-, beta- and gamma-synuclein. This protein is thought to be involved in neuronal plasticity because of its unique expression, mainly in the telencephalon during maturation. Consequently, disarrangement of NACP/alpha-synuclein might disrupt synaptic activity, resulting in memory disturbance. Previous studies have shown that damage to synaptic terminals is closely associated with global cognitive impairment and is an early event in the pathogenesis of Alzheimer's disease. Although the relationship between synaptic damage and amyloidogenesis is not clear, some proteins at the synaptic site have been implicated in both neuronal alteration and amyloid formation. Indeed, abnormal accumulation of both NACP/alpha-synuclein and Abeta precursor protein occurs at synapses of Alzheimer's patients. Other evidence suggests that NACP/alpha-synuclein is a component of the Lewy bodies found in patients with Parkinson's disease or dementia with Lewy bodies, and that a point mutation in this protein may be the cause of familial Parkinson's disease. Consequently, abnormal transport, metabolism or function of NACP/alpha-synuclein appears to impair synaptic function, which induces, at least in part, neuronal degeneration in several neurodegenerative diseases. The precursor of the non-amyloid β/A4 protein (non-Aβ) component of Alzheimer’s disease amyloid (NACP)/α-synuclein is the human homologue of α-synuclein, a member of a protein family which includes α-, β- and γ-synuclein. This protein is thought to be involved in neuronal plasticity because of its unique expression, mainly in the telencephalon during maturation. Consequently, disarrangement of NACP/α-synuclein might disrupt synaptic activity, resulting in memory disturbance. Previous studies have shown that damage to synaptic terminals is closely associated with global cognitive impairment and is an early event in the pathogenesis of Alzheimer’s disease. Although the relationship between synaptic damage and amyloidogenesis is not clear, some proteins at the synaptic site have been implicated in both neuronal alteration and amyloid formation. Indeed, abnormal accumulation of both NACP/α-synuclein and Aβ precursor protein occurs at synapses of Alzheimer’s patients. Other evidence suggests that NACP/α-synuclein is a component of the Lewy bodies found in patients with Parkinson’s disease or dementia with Lewy bodies, and that a point mutation in this protein may be the cause of familial Parkinson’s disease. Consequently, abnormal transport, metabolism or function of NACP/α-synuclein appears to impair synaptic function, which induces, at least in part, neuronal degeneration in several neurodegenerative diseases. |
| Author | Iwai, Akihiko |
| Author_xml | – sequence: 1 givenname: Akihiko surname: Iwai fullname: Iwai, Akihiko email: iwai@yamanouchi.co.jp organization: Neuroscience Research, Pharmacology Laboratories, Institute for Drug Discovery Research, Yamanouchi Pharmaceutical Co., Ltd., 21 Miyukigaoka, Tsukuba, Ibaraki 305-8585, Japan |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/10899435$$D View this record in MEDLINE/PubMed |
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| Keywords | Aβ, amyloid β/A4 protein PNP-14, phosphoneuroprotein 14 NAC, non-Aβ component of Alzheimer’s disease amyloid Synapse Alzheimer’s disease NACP, NAC precursor Synuclein Non-Aβ component of Alzheimer’s disease amyloid Parkinson’s disease ApoE, apolipoprotein E Lewy body APP, Aβ precursor protein |
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| Snippet | The precursor of the non-amyloid β/A4 protein (non-Aβ) component of Alzheimer’s disease amyloid (NACP)/α-synuclein is the human homologue of α-synuclein, a... The precursor of the non-amyloid beta/A4 protein (non-Abeta) component of Alzheimer's disease amyloid (NACP)/alpha-synuclein is the human homologue of... The precursor of the non-amyloid beta /A4 protein (non-A beta ) component of Alzheimer's disease amyloid (NACP)/ alpha -synuclein is the human homologue of... |
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| SubjectTerms | alpha-Synuclein Alzheimer Disease - genetics Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer’s disease Amino Acid Sequence Amyloid beta-Protein Precursor - analysis Animals Brain - metabolism Brain Chemistry Cerebral Cortex - chemistry Cerebral Cortex - pathology gamma-Synuclein Humans Lewy body Molecular Sequence Data Mutation Nerve Tissue Proteins - analysis Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Non-Aβ component of Alzheimer’s disease amyloid Parkinson Disease - genetics Parkinson’s disease Plaque, Amyloid - chemistry Sequence Alignment Synapse Synapses - chemistry Synuclein Synucleins |
| Title | Properties of NACP/α-synuclein and its role in Alzheimer’s disease |
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