Mitochondria
Alzheimer Disease
Amyloid Beta
β-Amyloid
Piron

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Amyloid Beta

https://en.m.wikipedia.org/wiki/Amyloid_beta

Amyloid beta, the core peptide that forms plaques in AD, potentiates tau toxicity and deposition into paired-helical filaments, ultimately conforming neurofibrillary tangles

https://www.sciencedirect.com/topics/medicine-and-dentistry/amyloid-beta

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Β-Amyloid Deposits in Young COVID Patients

https://papers.ssrn.com/sol3/papers.cfm?abstract_id=4003213

Beta-amyloid deposits found in young patients with COVID-19

https://www.news-medical.net/news/20220125/Beta-amyloid-deposits-found-in-young-patients-with-COVID-19.aspx

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Mitochondria as a Therapeutic Target for the Treatment of Alzheimer’s Disease

https://www.sciencedirect.com/science/article/pii/B9780128028100000106

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Alzheimer’s disease (AD) is the most common cause of dementia in the elderly and is characterized by the accumulation of neurofibrillary tangles and amyloid plaques in the brain, resulting in neuronal and synaptic dysfunction. Buildup of amyloid peptides (Aβ), a major component of amyloid plaques, can adversely affect mitochondria and promote metabolic dysfunction, thereby implicating mitochondria in AD pathogenesis.

Amyloid beta (Aβ or Abeta) denotes peptides of 36–43 amino acids that are the main component of the amyloid plaques found in the brains of people with Alzheimer's disease, leading to a chain reaction akin to a prion infection. The oligomers are toxic to nerve cells. The other protein implicated in Alzheimer's disease, tau protein, also forms such prion-like misfolded oligomers.