Alzheimer’s : New Drug Found
A new drug, Gantenerumab, shows promise in slowing early-onset Alzheimer’s while significantly reducing amyloid plaque buildup, a key marker of the disease.
- Alzheimer’s disease is a progressive neurodegenerative disorder that primarily affects memory, thinking, and reasoning abilities.
- It is the most common cause of dementia, accounting for 60-80% of all dementia cases
- The disease disrupts communication between brain cells, leading to a decline in cognitive and functional abilities.
- Early-Onset Alzheimer’s occur in individuals aged 65 or older, but around 5-10% of cases develop before this age—this is called Early-Onset Alzheimer’s Disease (EOAD).
- Unlike late-onset Alzheimer’s, EOAD progresses more rapidly and often affects people in their prime working years, making it particularly devastating.
- Genetic factors play a crucial role in early-onset cases, with mutations in three specific genes—APP, PSEN1, and PSEN2—linked to increased risk.
- The buildup of amyloid beta proteins in the brain leads to the formation of amyloid plaques, a hallmark of Alzheimer’s disease.
- These plaques disrupt neural communication, trigger inflammation, and eventually lead to brain cell death.
- Amyloid-targeting therapies aim to reduce these plaques, potentially slowing disease progression.
Gantenerumab:
- Gantenerumab is an experimental drug that was initially discontinued but has now shown promise in new clinical trials.
- The latest trial focused on patients with genetic mutations known to cause early-onset Alzheimer’s.
- It was a randomized, placebo-controlled study, tracking disease progression using brain imaging and blood biomarkers.
- Results showed a significant reduction in amyloid plaque buildup, suggesting the drug may slow cognitive decline.
