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ALZHEIMER’S DISEASE

ALZHEIMER’S DISEASE

New research in Alzheimer’s Disease (AD) has highlighted the role of microglia, unique brain macrophage-like cells responsible for “elimination of microbes, dead cells, redundant synapses, protein aggregates” and other particulates that may endanger the CNS.[1] In its complex role, however, this immune cell is implicated in significant neuroinflammation.

Alzheimer’s Disease (AD) is a neurodegenerative illness that in 2020 was diagnosed in 5.8 million Americans. Typically increasing with age, AD affects 1 in 9 people aged 65 and older. AD has long been associated with the accumulation of amyloid-beta protein that triggers the “abnormal deposition” of tau, a protein inside of brain neurons. Tangles of tau inside the neurons disrupt synaptic communication and lead to cell death.

Microglia [2] and other defences within the innate immune system of the brain work to protect cells and retain homeostasis. New research, however, implicates microglia and the gene responsible for it, CD33, in excessive neuroinflammation – a feature of other neurodegenerative illnesses such as ALS.

The presence of tau sends microglia and other immune mechanisms into overdrive, resulting in the inflammatory immune response…[3] contributing to cognitive decline and nerve death. The amyloid and tau start a fire that is intensified by the activated microglia.

This phenomenon of ‘killer’ microglia is downstream of the initial problem which is the accumulation of the amyloid and tau proteins. But what causes this accumulation? Part of the answer is genetics.

In the 1980s, neuroscientist Dr. Rudolph Tanzi discovered the “amyloid protein precursor” (APP) gene involved in the production of the amyloid beta-protein/amyloid A4 peptide – a protein present in the neuritic plaques and neurofibrillary tangles in the brains of patients with Alzheimer’s disease.[4] 30 genes have since been discovered for AD that include Presenilin 1 (PSEN1) and Presenilin 2 (PSEN2). Mutations in these genes are linked to high levels of amyloid and early onset Alzheimer’s. 

Listen to Dr. Tanzi: https://youtu.be/J5owaSenTqE

However, according to Dr. Tanzi, the amyloid protein is not “junk”. He suggests that the protein is actually anti-microbial and its formation triggered by the presence of bacteria, fungi or viruses. The amyloid forms to envelop the microbe. However, once the defensive protein forms and neurons begin to die, the mycroglia become over active. The microglia ‘assume’ that there is a spreading infection and begin destroying the ‘compromised’ parts of the brain.

Treatment for Alzheimer’s patients is about controlling the neuro inflammation (and oxidative stress) caused by the plaque and the aggressive immune response. New published research on this hyper-response of microglia and its genetic ‘on-off switch’ CD33 have found hope in TREM2, a gene that can balance and manage the expression of CD33.

In his work, Dr. Tanzi stresses the importance of primary prevention which starts decades before AD symptoms may emerge. Prevention includes identifying microbes that may gain access to the brain and genetics that predispose to the amyloid accumulation. It also includes lifestyle choices and exercise.

 

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NOTES

[1] https://www.annualreviews.org/doi/abs/10.1146/annurev-immunol-051116-052358

[2] https://www.frontiersin.org/articles/10.3389/fncel.2018.00488/full

[3] https://www.medscape.com/viewarticle/967592

[4] https://www.nature.com/articles/331528a0

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