Every day, hundreds of families hear the same heartbreaking words: “It’s Alzheimer’s.” For many, that moment divides life into before and after.

When I was diagnosed early, I counted myself among the lucky ones. Early detection opened a small window of choice, and with it, the possibility of hope. Two new treatments, Leqembi and Kisunla, now offer a chance to slow Alzheimer’s progression for those in the early stages. Choosing between them felt like standing at a fork in the road; one that could shape how much of me I get to keep.  Below is the information I wish I had known at the time – July 2024.

 Understanding Alzheimer’s

Before deciding, it is good to understand exactly what we are fighting.  Alzheimer’s begins quietly, when the brain can’t properly clear beta-amyloid and tau proteins. Normally, beta-amyloid and tau proteins have positive functions and are regularly cleared via our glymphatic system.  The glymphatic system, is a wonderful a network of channels in the brain that plays a crucial role in clearing waste products and other substances from the central nervous system like a filtration system flushing out impurities from water.

Alzheimer’s disease begins deep within the brain’s delicate balance of proteins. In its earliest stages, the system responsible for regulating beta-amyloid begins to falter, leading to an overproduction of these proteins. Instead of being cleared away, the excess beta-amyloid drifts through the spaces between neurons, where it begins to clump into sticky plaques too big to be swept away. Over time, these plaques block the communication pathways between brain cells, disrupting the electrical signals that carry thought, memory, and emotion.

 Inside the neurons, another battle unfolds. Here, tau proteins, which normally help maintain the cell’s internal structure, begin to twist into tangles. These tangles choke off nutrients and energy, starving the cell from within until it can no longer function.

The relationship between beta-amyloid and tau is both intimate and destructive. Beta-amyloid appears to act as the spark, setting off the misfolding of tau proteins inside the neuron. As tau becomes tangled, it worsens the damage beta-amyloid has already begun, creating a vicious cycle that accelerates neurodegeneration.

This dual assault, inside and outside the neurons, explains why Leqembi and Kisunla, two breakthrough Alzheimer’s treatments, focus on targeting beta-amyloid. Because these plaques are formed outside the neurons, they are more accessible to therapy, and removing them may slow or prevent the cascade that leads to tau tangles within the cells.

Bit by bit, if left unchecked, the plaques and tangles spread through the brain, silencing neural connections. What begins as a molecular imbalance grows into the erosion of memory, the fading of clarity, and the slow unraveling of identity: the very essence of who we are.

 A Look at Leqembi and Kisunla

 Leqembi and Kisunla are designed to target those destructive proteins. They are monoclonal antibodies, treatments that “tag” beta-amyloid so it can be broken down and cleared away by the glymphatic system. But they differ in how, and when, they attack.

  Kisunla zeroes in on a particularly toxic form of beta-amyloid called N-truncated pyroglutamate Aβ (N3pE-Aβ), a potent “seed” that can accelerate plaque growth.

 Leqembi, on the other hand, targets earlier and smaller forms of beta-amyloid, oligomers and protofibrils, the building blocks that eventually harden into plaque, it also targets plaques that have already formed. In essence, Leqembi acts both before and after plaque formation, clearing what’s harmful while preventing new damage.

Another difference lies in treatment duration. Kisunla’s current approach allows patients to stop treatment once PET scans show that plaques have been greatly reduced, much like ending chemotherapy when cancer cells are no longer visible. It’s still a new strategy, and time will tell whether re-treatment might be needed when amyloid plaque returns. Leqembi, in contrast, offers continuity. After 18 months of infusions every two weeks, patients may be able to move to monthly maintenance dosing, an ongoing effort to keep the brain clear of toxic proteins before they have a chance to cause more damage.

 Like all progress, though, these treatments come with risks. Both drugs can cause ARIA. Amyloid-Related Imaging Abnormalities, which may appear as swelling and/or bleeding in the brain. Most cases are mild and temporary, but the difference in risk is worth noting:

·        Leqembi: ARIA-E (12.6%) and ARIA-H (17.3%)

·        Kisunla: ARIA-E (24%) and ARIA-H (31.4%)

 Note: These %s indicate the percentage of patients in the original tests who got ARIA.  ARIA-E = swelling; ARIA-H = bleeding

Neither treatment stops the brain from over producing beta-amyloid: and that, for now, remains the core of the disease. 

 I chose Leqembi because it offers a broader, more sustained defense — targeting amyloid at multiple stages and maintaining that vigilance over time, with a lower risk of ARIAI.

If costs of continuing treatment are a consideration, Kisunla offers an end to treatment, and a similar initial clearing of beta-amyloid plaque as Leqembi. After 18 months, Leqembi patients can go on maintenance infusions once a month rather than every two weeks or the option of starting maintenance treatment with LEQEMBI IQLIK . It’s a single-use, pen-like injection given under the skin (a subcutaneous injection) by you or a care partner.

A special note:  The first Alzheimer’s related blood test I took in February of 2024 showed my Beta-amyloid 42/40, p-Tau181  and p-Tau217 tests all indicated mild cognitive impairment.  After my 28th infusion  and a recent blood test there has been significant improvement in the numbers that indicate a reversal of abnormal protein levels moving them in to the normal range and can be a strong indicator of a healthier brain state.  I believe this reversal is due to Leqembi.

 It’s not a cure, but it feels like momentum, a way to keep hold of myself a little longer, to preserve the connections that make life meaningful.  And in the end, that’s what hope looks like: the chance to stay you for as long as possible, while science continues to search for what comes next.

 If you are looking for insights that will empower and support you through your Alzheimer’s journey, you might find this book helpful:  Use Your Brain to Fight Alzheimer’s