As one grows older, we become aware of various maladies such as arthritis, type 2 diabetes, and other health challenges. Remembering how many of my older, now deceased, relatives lost their earlier cognitive skills, Alzheimer's is a risk but there is an approved, experimental treatment: LEQEMBI LEQEMBI (lecanemab) is an FDA-approved monoclonal antibody treatment for early Alzheimer's disease (mild cognitive impairment or mild dementia) that targets and removes amyloid plaques from the brain, slowing cognitive decline by reducing plaque buildup, with administration via IV infusion or at-home injection (LEQEMBI IQLIK). Key points include: it's for early stages, requires amyloid confirmation, slows decline (not a cure), has side effects like brain swelling/bleeding (ARIA), and is covered by Medicare for eligible patients, though costs vary. What it is & how it works Type: A monoclonal antibody (lecanemab). Action: Targets and clears beta-amyloid plaques in the brain, a hallmark of Alzheimer's. Purpose: Slows the progression of cognitive and functional decline in early Alzheimer's. Who is eligible Adults with mild cognitive impairment or mild dementia due to Alzheimer's. Must have confirmed amyloid plaques in the brain via diagnostic tests and imaging. Administration IV Infusion: Given by a healthcare professional. LEQEMBI IQLIK: An approved, single-use injection for at-home self-administration (thigh/abdomen/back of arm). Potential side effects (ARIA) Amyloid-Related Imaging Abnormalities (ARIA) are common, usually temporary brain swelling (ARIA-E) and small spots of bleeding (ARIA-H). Symptoms can include headache, confusion, dizziness, vision changes, nausea, or seizures, but often people have no symptoms. Serious or life-threatening ARIA can occur. Cost & coverage Medicare covers Leqembi for eligible patients. Annual costs can be significant (around $26,500 for the drug), with patient copays often around 20%. Important note It is not a cure for Alzheimer's, but a treatment to slow the disease's progression, allowing more time for daily life. At $26,000, that would be half of my Social Security. Regardless, I was clued by: Dang Canadian, socialized medicine. They get all the good stuff at affordable rates. A more technical description until good Prius friend @tochatihu joins the thread: Bob Wilson
This stuff is treating a symptom and not a cause... It's like your car's oil pressure light is on and you're modifying that warning light so it's 9% less bright without actually finding out why there's no oil pressure. In this case the cerebrospinal fluid that pumps up your spine and washes your brain during deep sleep is being ignored and less plaque in the brain by others means was developed. There's so much more science that has advanced to deal with Alzheimer's and this ain't one of them. Sadly the RX industry cares more about what they can sell for money than actually finding a more viable approach that isn't as much of a waste of money. Abstract On July 6, 2023, the U.S. Food and Drug Administration (FDA) approved lecanemab (Leqembi) for the treatment of Alzheimer’s dementia (AD) patients. In 2 clinical trials, lecanemab reduced amyloid in the brain and slowed cognitive decline. Here, I review in detail the clinical trial by van Dyck et al. (2023) entitled “Lecanemab in early Alzheimer’s disease”, published in The New England Journal of Medicine on January 5, 2023. In this 18-month trial, lecanemab did not slow cognitive decline in women. This is especially significant because women have a twofold increased risk of AD compared to men, that is, there are 2 times more women than men living with AD. Lecanemab did not slow cognitive decline in APOE4 carriers; rather, it enhanced the decline in study participants with 2 APOE4 genes. This is bad news for AD patients, 60–75% of whom carry at least 1 APOE4 gene. These negative results regarding lecanemab’s therapeutic value make me wonder if the approval of lecanemab was the worst decision of the FDA up till now, after the approval of aducanumab on June 7, 2021. Advances in Clinical and Experimental Medicine
"A more technical description ..." I knew nothing of this monoclonal antibody (MCA) until reading here. Based on general knowledge, this MCA crosses the blood brain barrier which implies it is a small molecule. By mechanism not (here) described it slows accumulation of amyloid plaques. As it can mess up other amyloid things, it is a somewhat blunt tool. But afaik none others exist. In a general sense, I am interested in immune function on the 'safe side' of brain's blood barrier, because cells ought not pass. Maybe everything is built on the safe side. Some medical drs would know. But no cells anywhere can be without immune protection. Would have been evolved out very long ago. Now that it is on the market, efficacy will become better known and poorer performance in females. == "It's like your car's oil pressure light is on and you're modifying that warning light so it's 9% less bright without actually finding out why there's no oil pressure." This is not an impressive analogy because dimming the warning light is unrelated to engine internal friction.
