Amyloid-Beta and Phosphorylated Tau Accumulations Cause Abnormalities at Synapses of Alzheimer’s disease Neurons
| العنوان: | Amyloid-Beta and Phosphorylated Tau Accumulations Cause Abnormalities at Synapses of Alzheimer’s disease Neurons |
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| المؤلفون: | Ravi Rajmohan, P. Hemachandra Reddy |
| المصدر: | Journal of Alzheimer's Disease. 57:975-999 |
| بيانات النشر: | IOS Press, 2017. |
| سنة النشر: | 2017 |
| مصطلحات موضوعية: | 0301 basic medicine, Amyloid, Amyloid beta, tau Proteins, Disease, Neurotransmission, Article, Synapse, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Alzheimer Disease, mental disorders, medicine, Animals, Humans, Phosphorylation, Neurotransmitter, Amyloid beta-Peptides, biology, General Neuroscience, General Medicine, medicine.disease, Psychiatry and Mental health, Clinical Psychology, 030104 developmental biology, chemistry, Synapses, biology.protein, Axoplasmic transport, Geriatrics and Gerontology, Alzheimer's disease, Psychology, Neuroscience, 030217 neurology & neurosurgery |
| الوصف: | Amyloid Beta (Aβ) and hyperphosphorylated tau are hallmark lesions of Alzheimer disease (AD). However, the loss of synapses and dysfunctions of neurotransmission are more directly tied to disease severity. The role of these lesions in the pathoetiological progression of the disease remains contested. Biochemical, cellular, molecular and pathological studies provided several lines of evidence and improved our understanding of how amyloid beta and hyperphosphorylated tau accumulation may directly harm synapses and alter neurotransmission. In-vitro evidence suggests that amyloid beta and hyperphosphorylated tau have both direct and indirect cytotoxic effects that affect neurotransmission, axonal transport, signaling cascades, organelle function, and immune response in ways that lead to synaptic loss and dysfunctions in neurotransmitter release. Observations in preclinical models and autopsy studies support these findings, suggesting that while the pathoetiology of positive lesions remains elusive, their removal may reduce disease severity and progression. The purpose of this article is to highlight the need for further investigation of the role of tau in disease progression and its interactions with Aβ and neurotransmitters alike. |
| تدمد: | 1875-8908 1387-2877 |
| DOI: | 10.3233/jad-160612 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::dd32adaf9ebcb02fe788d2c44023ed25 https://doi.org/10.3233/jad-160612 |
| Rights: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....dd32adaf9ebcb02fe788d2c44023ed25 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 18758908 13872877 |
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| DOI: | 10.3233/jad-160612 |