Synaptic basis of Alzheimer's disease: Focus on synaptic amyloid beta, P-tau and mitochondria
John A, Reddy PH.. Ageing research reviews, 2020-11-04
Topic: Amyloid, tau and blood-test diagnosis
Alzheimer's disease (AD) is a progressive and synaptic failure disease. Despite the many years of research, AD still harbors many secrets. As more of the world's population grows older, researchers are striving to find greater information on disease progression and pathogenesis. Identifying and treating the markers of this disease, or better yet, preventing it all together, are the hopes of those investing in this field of study. Several years of research revealed that synaptic pathology and mitochondrial oxidative damage are early events in disease progression. Loss of synapses and synaptic damage are the best correlates of cognitive deficits found in AD patients. As the disease progresses, there are significant changes at the synapse. These changes can both shed greater light onto the progression of the disease and serve as markers and therapeutic targets. This article addresses the mechanisms of synaptic action, mitochondrial regulation/dysregulation, resulting synaptic changes caused by amyloid beta and phosphorylated tau in AD progression. This article also highlights recent developments of risk factors, genetics and ApoE4 involvement, factors related to synaptic damage and loss, mislocalization of amyloid beta and phosphorylated tau, mitophagy, microglial activation and synapse-based therapies in AD. Furthermore, impairments in LTD and reactivation of microglia are discussed.
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APA 7th
John, A., & Reddy, P. H. (2021). Synaptic basis of Alzheimer's disease: Focus on synaptic amyloid beta, P-tau and mitochondria. Ageing research reviews. https://doi.org/10.1016/j.arr.2020.101208
Vancouver
John A, Reddy PH. Synaptic basis of Alzheimer's disease: Focus on synaptic amyloid beta, P-tau and mitochondria. Ageing research reviews. 2021. doi:10.1016/j.arr.2020.101208. PMID: 33157321.
BibTeX
@article{john2021-33157321,
author = {John, A. and Reddy, P. H.},
title = {{Synaptic basis of Alzheimer's disease: Focus on synaptic amyloid beta, P-tau and mitochondria}},
journal = {Ageing research reviews},
year = {2021},
doi = {10.1016/j.arr.2020.101208},
pmid = {33157321},
url = {https://doi.org/10.1016/j.arr.2020.101208}
}
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Key findings
- Several years of research revealed that synaptic pathology and mitochondrial oxidative damage are early events in disease progression.
- As the disease progresses, there are significant changes at the synapse.
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Study details
- Evidence strengthLow
How this study scored 40/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 23 of the 58 points we could judge it on, which is 40 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Ageing research reviews) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 3 / 5 | 2021 — within 6 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 33157321) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 23 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 23 of the 58 points we could judge it on is 40 out of 100. |
| Total | 40 / 100 | — |
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