spring newsletter

In This Issue:

  • Anti-Tau Therapies
  • Alzheimer's Association Facts and Figures 2022
  • New Additions to the Easton Center
  • Clinical Trials
  • Upcoming Events

The Mary S. Easton Center for Alzheimer’s Disease Research at UCLA has very active teams working on basic research, drug discovery, biomarkers for early diagnosis and clinical activity including clinical trials, cognitive testing, and patient care.


Anti-Tau Therapies

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By: Maryam Beigi, MD​

Alzheimer’s Disease is leading cause of dementia worldwide, and its prevalence is expected to double in the next 20 years. Clinical presentations include loss of memory, language or visual processing abilities, as well as neuropsychiatric symptoms such as apathy, depression, anxiety, agitation, and psychosis.

At autopsy, the brains of patients who lived with Alzheimer’s disease contain amyloidbeta plaques outside of cells and tau neurofibrillary tangles (NFT) inside of cells, along with extensive loss of neuronal synapses.

Scientists have postulated that these two proteins (amyloid-beta and tau), either alone or in combination cause disease initiation and progression. In our last newsletter I described the formation of amyloid-beta from the amyloid precursor protein (APP). The process of amyloid beta deposition in the brain starts 15-20 years before a person becomes symptomatic. Once symptoms of Alzheimer’s begin, the tau protein begins to aggregate at an accelerated pace.

Tau is a protein that binds to the highways within neurons for transportation of molecules. These highways can extend over a thousand times the size of the cell body. Tau supports the skeleton that holds these highways together inside neurons. Excess chemical modifications of tau (i.e. phosphorylation) are thought to cause the breakdown and collapse of the cellular skeleton,

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