amyloid，tau蛋白看来确实会引起老年痴呆

[Mountainlion]

When one member of a large Colombian family, plagued by Alzheimer’s disease for generations, evaded the disease (staying cognitively healthy into her 70s) despite inheriting the genetic mutation that caused her relatives to develop dementia in their 40s, researchers sought to understand why.

The Colombian patient carried the presenilin-1 mutation. Generally, people with a presenilin-1 mutation (PSEN1-E280A) develop amyloid buildup beginning in their 20s, accumulate amyloid quickly, and typically start showing signs of cognitive decline in middle age. However, the patient was also a homozygous carrier of the APOE3 Christchurch (APOE3ch) mutation which is thought to provide resistance to Alzheimer’s disease.

“One of the biggest unanswered questions in the Alzheimer’s field is why amyloid accumulation leads to tau pathology,” said David Holtzman, MD, professor of neurology at Washington University School of Medicine. “This woman was very, very unusual in that she had amyloid pathology but not much tau pathology and only very mild cognitive symptoms that came on late. This suggested to us that she might hold clues to this link between amyloid and tau.”

In a new study, researchers used genetically modified mice to show that the Christchurch mutation severs the link between the early phase of Alzheimer’s disease, amyloid beta builds up in the brain, and the late phase, when tau accumulates and cognitive decline sets in.

This work is published in Cell in the paper, “APOE3ch alters microglial response and suppresses Aβ-induced tau seeding and spread.”https://www.cell.com/cell/fulltext/S009 ... 3Dtrue#%20

[wdds]

没理解，饮食上如何注意？

[changjiang]

When one member of a large Colombian family, plagued by Alzheimer’s disease for generations, evaded the disease (staying cognitively healthy into her 70s) despite inheriting the genetic mutation that caused her relatives to develop dementia in their 40s, researchers sought to understand why.

The Colombian patient carried the presenilin-1 mutation. Generally, people with a presenilin-1 mutation (PSEN1-E280A) develop amyloid buildup beginning in their 20s, accumulate amyloid quickly, and typically start showing signs of cognitive decline in middle age. However, the patient was also a homozygous carrier of the APOE3 Christchurch (APOE3ch) mutation which is thought to provide resistance to Alzheimer’s disease.

“One of the biggest unanswered questions in the Alzheimer’s field is why amyloid accumulation leads to tau pathology,” said David Holtzman, MD, professor of neurology at Washington University School of Medicine. “This woman was very, very unusual in that she had amyloid pathology but not much tau pathology and only very mild cognitive symptoms that came on late. This suggested to us that she might hold clues to this link between amyloid and tau.”

In a new study, researchers used genetically modified mice to show that the Christchurch mutation severs the link between the early phase of Alzheimer’s disease, amyloid beta builds up in the brain, and the late phase, when tau accumulates and cognitive decline sets in.

This work is published in Cell in the paper, “APOE3ch alters microglial response and suppresses Aβ-induced tau seeding and spread.”https://www.cell.com/cell/fulltext/S009 ... 3Dtrue#%20

Cool. Looks like highly important finding for the field.