Alzheimer's disease is a neurodegenerative disease that usually starts slowly and progressively worsens, & is the cause of 60–70% of cases of dementia. The most common early symptom is difficulty in remembering recent events. As the disease advances, symptoms can include problems with language, disorientation (including easily getting lost), mood swings, loss of motivation, self-neglect, & behavioral issues. As a person's condition declines, they often withdraw from family & society. Gradually, bodily functions are lost, ultimately leading to death. Although the speed of progression can vary, the average life expectancy following diagnosis is three to twelve years.
In Australia, approximately 1,700 to 1,800 new cases of dementia are diagnosed every week (which equate to roughly one person every 6 minute). Because Alzheimer's disease is the most common form of dementia—accounting for up to 70% of all cases—this means that between 1,200 & 1,260 Australians are diagnosed specifically with Alzheimer's every single week. The Broader Australian Context Data from the Australian Institute of Health and Welfare (AIHW) & Dementia Australia highlight these weekly numbers are rising so quickly: Leading Cause of Death: Dementia has officially surpassed coronary heart disease to become the leading cause of death for Australians. Total Prevalence: There are an estimated 446,500 Australians living with all form of dementia. The Aging Population Surge: Because Australia has an aging population, that weekly diagnosis rate is expected to skyrocket over the coming decades. By 2065, the total number of Australians living with dementia is projected to surge past 1 million all because of processed food & a booming sugar industry .
Amyloid plaques build up in Alzheimer's brains . Obesity increases 3x the risk of Alzheimer's Plaques form when protein pieces called beta-amyloid clump together. Beta-amyloid comes from a larger protein found in the fatty membrane surrounding nerve cells. Beta-amyloid is chemically "sticky" and gradually builds up into plaques. Beta amyloids comes from LDH cholesterol Amyloid beta (Aβ or Abeta) denotes peptides of 36–43 amino acids that are the main component of the amyloid plaques found in the brains of people with Alzheimer's disease. The peptides derive from the amyloid-beta precursor protein (APP), which is cleaved by beta secretase and gamma secretase to yield Aβ in a cholesterol-dependent process and substrate presentation. Beta-amyloid comes from a larger protein found in the fatty membrane surrounding nerve cells. Beta-amyloid is chemically "sticky" and gradually builds up into plaques. The brain shrinks with age due to a lack of HDL high density lipo protein omega 3 Although a unified theory for microbial colonization of the brain has not been formed, multiple research groups have suggested ways this occurs. Weber et al noted that specific species of bacteria identified in studies exploring the brain microbiome in AD are normally found in the oral microbiome. Therefore, they hypothesized, that pathogenic changes in the oral cavity (often seen in AD) may damage connective tissues. This tissue destruction releases bacteria from the oral cavity, allowing for nervous system infection. Some of these bacteria can create a biofilm, through the production of amyloid proteins. These bacterial amyloids share similarities to the disease-causing versions.13 These amyloids may then allow other native amyloid proteins to aggregate and form colonies, beginning the pathogenesis of AD. Silica removes plaque deposits on nerve endings Aluminum out of the brain allowing for quick clear brain signals. to prevent Alzheimer's ingest charcoal smoothies and own a hydrogen water bottle turns out fatty acids what the brain is made of are composed of carbon & Hydrogen the lack of minerals & carbon in the skull cause the skulls to thin with cavities to avoid this supplement with charcoal smoothies for carbon & drink gastroliths. Etanercept, the active ingredient used in perispinal administration (commonly branded as Enbrel), is a large, complex dimeric fusion protein with the chemical formula : C2224H3475N621O698S36. Key Structural & Formulation Detail: Structure: It is a dimeric, fully human soluble TNF receptor Fc fusion protein, consisting of 934 amino acids with a molecular weight of approximately 150 kilodaltons (kDa).Composition: Perispinal etanercept combine the extracellular ligand-binding portion of the human 75 kDa (p75) TNF receptor with the Fc portion of human IgG1. Perispinal Formulation: For perispinal administration, etanercept is typically prepared by solubilizing the lyophilized powder (25 mg vial) with 1.8 cc of sterile water, which often includes sucrose, sodium chloride, L-arginine hydrochloride, and sodium phosphate. Mechanism: Perispinal etanercept acts as a tumor necrosis factor (TNF) inhibitor, used in studies for neuroinflammation. Perispinal etanercept has miraculous heling effect on Alzheimer's patients .
In Alzheimer’s disease, the dramatic rise in TNF-alpha is driven by a state of chronic, runaway inflammation in the brain. While TNF-alpha is normally a helpful signaling protein that coordinate immune response & synaptic pruning, in an Alzheimer’s brain, it trapped in a vicious, destructive feedback loop. Here is the exact biochemical breakdown of why TNF-alpha spike & how it drive the disease forward: 1. The Microglia "Overdrive" Switch The primary source of TNF-alpha in the brain are microglia (the brain's resident immune cells) & astrocytes. The Trigger: In a healthy brain, microglia easily clear out metabolic waste. However, in sugar filled Alzheimer’s, abnormal protein—specifically amyloid-beta (Abeta) plaques & hyperphosphorylated tau tangles—accumulate in the extracellular space. The Receptor Binding: These misfolded protein bind directly to specific pattern on microglia (like Toll-like receptor, or TLRs). This binding act as a massive alarm bell, activating the master inflammatory protein complex NF-κB inside the cell. The Result: NF-κB immediately tells the microglia to aggressively manufacture & secrete massive quantity of TNF-alpha to destroy the perceived threat. 2. The Vicious Destructive Loop Instead of fixing the problem, the sudden flood of TNF-alpha trigger a catastrophic feedback loop: Upregulating BACE1: TNF-alpha binds to receptors on neurons and upregulate an enzyme called BACE1 (beta-secretase). BACE1 is the exact enzyme responsible for cutting amyloid precursor protein into more toxic amyloid-beta. The extra amyloid-beta form more plaques, which recruit & anger more microglia, pumping out even more TNF-alpha. 3. Synaptic Cutoff & Neurotoxicity as TNF-alpha level skyrocket in the extracellular space, it shift from a protective signal to a highly neurotoxic one: Excitotoxicity (Glutamate Overload): High concentration of TNF-alpha force astrocytes to stop absorbing glutamate (the brain's primary excitatory neurotransmitter) from the synaptic cleft. At the same time, it force neurons to pump more AMPA receptors to their surface. This flood neurons with excess calcium, leading to synaptic burnout & cell death. Blood-Brain Barrier Breakdown: TNF-alpha directly degrade the tight junction of the blood-brain barrier (BBB). As the barrier weaken, peripheral inflammatory cells & toxins from the rest of the body leak into the brain, further fueling the neuroinflammatory fire. The Clinical Connection Because TNF-alpha is such a central driver of this damage, it has become a major target for modern Alzheimer's research. Clinical data show that Alzheimer’s patients have highly elevated TNF-alpha level in both their cerebrospinal fluid & blood plasma which has led research to investigate whether anti-TNF therapy (biologics historically used for autoimmune condition like rheumatoid arthritis) can cross the blood-brain barrier to break this inflammatory cycle & slow down cognitive decline.
A second drug called Kisunla (donanemab) a complex monoclonal antibody protein, not a simple compound with a single chemical formula like water; its formula is approximately C6452H10038N1708O2013S42, representing its large peptide structure with pentose monosaccharide , with a molecular weight around 145 kDa, used to treat early Alzheimer's by targeting amyloid plaques. Because Lecanemab (marketed as Leqembi) is a humanized IgG1 monoclonal antibody rather than a typical small-molecule drug, its chemical composition reflect a massive, complex macro-glycoprotein structure empirical chemical formula is: C6544H10088N1744O2032S46 Structural & Molecular Property Molecular Weight: Approximately 147,180 g/mol (approx 147.2 kDa) CAS Registry Number: 1260393-98-3 Composition: It is a tetramer consisting of two identical immunoglobulin heavy chains (each composed of approximately 451 amino acids) and two identical kappa light chains (each composed of approximately 219 amino acids), interlinked by both intra- and inter-chain disulfide bonds S–S bridges indicated by the 46 sulfur atoms. As an antibody designed to target soluble amyloid-beta A beta protofibrils in early Alzheimer's disease progression, this massive molecular structure dictate pharmacokinetics—requiring intravenous delivery to bypass systemic degradation so rely on a tiny percentage of these large protein crossing the blood-brain barrier via passive diffusion. Xanamem C19H19N5O2S is a highly selective, brain-penetrant small molecule inhibitor of the enzyme 11beta-hydroxysteroid dehydrogenase type 1 11beta-HSD1. The Local Cortisol Cycle: While systemic cortisol is managed by the adrenal glands via the HPA axis, localized concentration within brain tissue are amplified by 11beta-HSD1. This enzyme convert inactive cortisone into active cortisol right inside brain cells (astrocytes & neurons). The Neurotoxic Loop: Chronically elevated intracellular cortisol is highly toxic to the hippocampus & frontal cortex. It drive neuro-inflammation, accelerate dendritic atrophy, impair synaptic plasticity & has been shown in animal model to accelerate the deposition of amyloid-beta & tau pathology. The Blockade: Xanamem cross the blood-brain barrier with high efficiency. Positron Emission Tomography (PET) imaging has shown that a low oral dose (10 mg/day) achieve near-saturation, reaching approximately 70% to 80% target occupancy across the neocortex & medial temporal lobes. By inhibiting 11beta-HSD1, it prevent the localized regeneration of cortisol without completely suppressing systemic plasma cortisol level, protecting the brain from steroid-induced metabolic damage. Neuralcim The Amino Acid Formula (Protein Backbone)Excluding the variable carbohydrate chains attached during cellular expression, the elemental empirical formula of the 165-amino-acid human erythropoietin polypeptide chain is: C815H1317N223O241S5 (commercially formulated as NeuralCIM® & scientifically known as NeuroEPO) is an intranasally administered neuroprotective drug developed by the Center for Molecular Immunology (CIM) in Havana, Cuba. Unlike small-molecule drugs (like Xanamem) or monoclonal antibodies targeting amyloid removal (like lecanemab), Neuralcim leverage a modified glycoprotein pathway to preserve brain tissue structure & metabolic integrity. 1. The Mechanism: What is NeuroEPO? Neuralcim is a recombinant human erythropoietin (EPO) variant, but with a critical molecular modification: it has a low sialic acid content. The Problem with Standard EPO: Regular erythropoietin is a hormone that stimulate red blood cell production (hematopoiesis). If you gave normal EPO systemically at the high dose required to cross into the brain, it would dangerously thicken the blood, causing stroke & blood clot. The Structural Solution: By engineering the protein to have low sialic acid, it mimic the specific structure of EPO naturally produced by brain support cells (astrocytes). This structural shift drastically shorten it half-life in the bloodstream, meaning it completely lack hematopoietic activity—it will not alter red blood cell count. Brain Delivery via the Nasal Pathway: Because it is delivered intranasally, the massive glycoprotein bypasse the blood-brain barrier by traveling directly along the olfactory & trigeminal nerve pathway into the cerebrospinal fluid & brain tissue. 2. Cellular Action in the Alzheimer's Brain Once inside the central nervous system, NeuroEPO bind to specialized EPOR (erythropoietin receptor) complexes on neurons and glial cells, launching a multi-pronged neuroprotective response: Inhibition of Apoptosis: It act as a direct biochemical survival signal, blocking cascade that trigger programmed cell death in metabolic or oxidatively stressed neurons. Mitigating Neuro-inflammation & Oxidative Stress: It downregulate pro-inflammatory cytokines and enhance localized antioxidant defense mechanism, preventing the free radical cascade that destroy synaptic networks. Neurogenesis & Synaptic Preservation: NeuroEPO has been shown to stimulate brain growth factors, encouraging structural remodeling (neuroplasticity) preventing the loss of vital synaptic connection between cells.
Lithium show promise for Alzheimer's prevention and treatment, with studies suggesting naturally lower levels are linked to increased risk, while supplementation, especially with specific salts like lithium orotate, might reduce amyloid plaques, tau tangles, and cognitive decline in mice, potentially by restoring brain lithium levels depleted by plaques. While some clinical trials are exploring low-dose lithium for agitation and cognition in AD, overall meta-analyses haven't confirmed broad effectiveness yet, highlighting the need for more research on specific lithium compounds and dosing for humans . Hypoperfusion in Alzheimer's refers to the reduced blood flow (oxygen/nutrients) to the brain, a key factor contributing to cognitive decline, linking vascular issues with AD pathology, causing white matter damage, inflammation, and amyloid/tau problems, and acting as an early sign or precursor, suggesting improving blood flow might help treatment. Chronic poor perfusion stresses brain cells, leading to neurodegeneration, affecting memory and function, and is often seen with vascular risk factors so take Albumin as a supplement to improve blood flow & stop drinking sugar & eating 95% carbs switch to a ketogenic diet of 5% carbs 95% protein & may your brain . Gut microbiota dysbiosis, or an imbalance in gut bacteria, is closely linked to the onset and progression of Alzheimer’s disease (AD). This imbalance promote systemic inflammation, disrupt the blood-brain barrier & accelerate the accumulation of amyloid-beta (Aβ) plaques and tau tangles via the gut-brain axis. Key Connection Between Dysbiosis and Alzheimer's Microbial Imbalance: AD patients often show a decrease in beneficial bacteria (e.g., Firmicutes, Bifidobacteria) and an increase in pro-inflammatory bacteria (e.g., Bacteroidetes, Proteobacteria).
The primary minerals scientifically proven to reduce the production & downstream effect of TNF-alpha (Tumor Necrosis Factor-alpha) are Zinc & Magnesium. Rather than blocking the TNF protein directly once it is already floating in the bloodstream, these minerals work at a cellular level by disrupting the inflammatory master-switch pathway that tell your immune cells to manufacture TNF in the first place. 1. Zinc (The Primary Signaling Interrupter) Zinc is one of the most potent natural inhibitor of pro-inflammatory cytokines like TNF-alpha. It reduce effect through a very specific biochemical pathway: Inhibition of NF-kB: Under normal inflammatory stress, a protein complex called NF-κB move into the nucleus of your immune cells (monocytes and macrophages) & turn on the genes that synthesize TNF-alpha. Zinc block this process by upregulating an inhibitory protein called A20, which essentially shut down the NF-κB pathway. The Raf-1/IKKβ Mechanism: Clinical study show that zinc elevate a signaling molecule called cGMP, which activate Protein Kinase A. This cascade selectively jam the intracellular signaling chain (specifically Raf-1 & IκB kinase beta), stopping the production of TNF-alpha right at the source. 2. Magnesium (The Systemic Stabilizer) Magnesium behave as a natural anti-inflammatory gatekeeper. Chronic low magnesium level are strongly correlated with elevated systemic TNF-alpha & C-Reactive Protein (CRP). Calcium Channel Regulation: When cellular magnesium is low, L-type calcium channels on your immune cells open up. An excess influx of calcium causes macrophages to go into overdrive & pump out massive amounts of TNF-alpha. Adequate magnesium stabilize these cell membranes, keeping the calcium gates regulated & suppressing cytokine release. PI3K/Akt Pathway Protection: Research show that magnesium form (like Magnesium L-Threonate or Glycinate) suppress glial & systemic inflammation by upregulating the PI3K/Akt survival pathway, which keep immune cells in a resting, non-destructive state. Secondary Trace Minerals While Zinc & Magnesium do the heavy lifting, two other trace minerals play an essential supporting role by acting as cofactor for the body's natural antioxidant system, preventing the oxidative stress that trigger TNF release: Selenium: Essential for creating glutathione peroxidase. Selenium deficiency allow oxidative damage to run rampant, which trigger a secondary spike in TNF-alpha production. Copper: Work in tandem with zinc to form Copper-Zinc Superoxide Dismutase (CuZn-SOD), an enzyme that neutralize free radicals before they can provoke an inflammatory TNF cascade. If you are looking to address systemic inflammation or a specific autoimmune pathway, a combination of Zinc (balanced with a tiny fraction of copper to prevent deficiency) & highly bioavailable Magnesium (like Glycinate, Malate, or Threonate) provide the most robust nutritional defense against elevated TNF activity.
In the context of Alzheimer’s disease, the disruption of microtubules a central event that lead to the breakdown of communication within brain cells (neurons). Microtubules are essentially the "railway tracks" of the cell, providing structural support a transport system for essential nutrients & molecules. The Role of Tau Protein In a healthy neuron, a protein called **tau** act like the "railroad ties" that hold the microtubule tracks together. It stabilize the microtubules so they can function properly. In Alzheimer’s disease, however, chemical change cause tau to malfunction: Hyperphosphorylation: Tau proteins collect too many phosphate groups, causing them to change shape. **Detachment:** These altered tau protein detach from the microtubules. Without tau to hold them together, the microtubules **collapse & disintegrate**. Aggregation: The loose tau proteins then stick to each other, forming "neurofibrillary tangles" inside the neuron. The hyperphosphorylation of tau protein in Alzheimer’s disease is a result of a massive breakdown in the cell's chemical regulatory system. In a healthy brain, phosphate groups are added & removed from tau to control its activity, but in Alzheimer’s, this balance is lost. The primary reasons for this "runaway" phosphorylation include: 1. Kinase & Phosphatase Imbalance The chemical state of tau is managed by two type of enzymes **Kinases** These add phosphate groups (phosphorylation). **Phosphatases** These remove phosphate groups (dephosphorylation). In Alzheimer’s, **kinases** specifically GSK3beta & CDK5 become overactive, while **phosphatases such as PP2A become sluggish. This result in tau proteins that are "over-decorated" with phosphate groups, causing them to lose their shape & detach from microtubules .2. The Influence of Amyloid-Beta Current research suggest a "cross-talk" between the two hallmark pathology of Alzheimer's. The accumulation of amyloid-beta plaques outside the neuron can trigger signaling pathways that activate the kinases mentioned above. Essentially, the presence of plaques send a "stress signal" into the cell that lead to tau hyperphosphorylation .3. Oxidative Stress & Neuroinflammation As we age or face neurodegenerative condition, the brain experience increased oxidative stress. This environment damage cellular component & disrupt the metabolic pathways that keep enzymes in check. Inflammation: Microglia (the brain's immune cells) release pro-inflammatory cytokines that further stimulate kinase activity, creating a feedback loop that accelerate tau damage .4. Glucose Metabolism Issue Some research refer to Alzheimer’s as "Type 3 Diabetes" because [increased glucose metabolism] in the brain is linked to tau changes don't drink sugar drink minerals . When the brain cannot process glucose efficiently or when the brain is over fed sugar, it affect a process called **O-GlcN Acylation**, which normally compete with phosphorylation. If O-GlcN Acylation drop, phosphorylation sites on the tau protein become "open," making it much easier for kinases to over-saturate the protein with phosphate. Summary of the Process 1. 1. Enzyme Mismanagement Too many "adders" (kinase) not enough "removers" (phosphatase).
2. Structural Collapse: The negative charge from the extra phosphate cause tau to repel the microtubule & stick to other tau proteins.
3. Tangle Formation: These detached protein clump into Neurofibrillary Tangles (NFTs), which are toxic to the neuron.
Consequences of Disruption When these microtubule "tracks" vanish, the neuron faces several catastrophic failure: 1. Transport Failure
Neurons are often very long. They rely on microtubules to move protein & neurotransmitters from the cell body to the synapse (the communication point). When microtubules disrupt, this supply chain break down & the cell effectively starves or fail to send signals.
2. Synaptic Loss Because the neuron can no longer transport necessary material to its ends, the connection between neurons (synapses) begin to wither. This is the primary driver of the memory loss or cognitive decline seen in patients.
3. Cell Death The accumulation of tau tangles & the loss of internal structure eventually trigger pathways that lead to the death of the neuron. As more neurons die, the brain physically shrink (atrophy).
Research & Potential Treatment Because microtubule disruption happen relatively early in the disease process, research is looking for ways to intervene: Microtubule-Stabilizing Drugs: Some experimental therapy aim to use chemicals that can mimic the role of tau to keep the "tracks" intact even when tau fails. Tau-Targeted Therapy: Other approaches focus on preventing tau from becoming hyperphosphorylated or clearing out the tangles before they can cause damage.
Heparan Sulfates (HS) cover the surface of brain cells like a dense biochemical mesh. These chains are stabilized by disulfide bonds (bridges formed between sulfur-containing amino acids, like cysteine). If these internal sulfur bridges are disrupted, the TNF-alpha protein unravel, rendering it completely inert & unable to bind to cell receptors. Sulfate act as a brake: In a young, healthy brain, highly sulfated heparan sulfate bind directly to the BACE1 enzyme (the enzyme responsible for cutting protein into toxic amyloid-beta plaques) & naturally inhibit it. It act as a safety brake to keep plaque formation low. The aging breakdown: As the brain age or develop Alzheimer’s, genetic shift cause a significant loss of sulfate on these pentose chains (a decrease in 6-O-sulfation). The TNF connection: Without these highly sulfated chains, the safety brake is lost, allowing BACE1 activity to skyrocket. As established, TNF-alpha directly upregulate BACE1. When you combine a high-TNF environment with a low-sulfate brain, BACE1 run completely wild, rapidly accelerating the production of amyloid plaque & fueling the neuroinflammatory loop.
Neuroinflammation: Reduced level of protective, short-chain fatty acids (SCFAs) like butyrate, alongside increased bacterial toxins (lipopolysaccharides, or LPS), lead to chronic inflammation that damage neurons. Blood-Brain Barrier (BBB) Dysfunction: Dysbiosis increase intestinal permeability, allowing bacteria-derived products to enter the bloodstream and enter the brain, promoting neuroinflammation. The APOE4 Link: Carriers of the APOE4 gene, the strongest genetic risk factor for Alzheimer's, exhibit a distinct, more pro-inflammatory gut microbiome, even before cognitive decline. Potential Therapeutic Strategy
Probiotics/Prebiotics: Introducing beneficial bacteria (e.g., Lactobacillus, Bifidobacterium) can improve cognitive function and reduce amyloid-beta in animal models. Dietary Adjustment: Diet play a major role in shaping the microbiome and can be used to mitigate inflammation. Fecal Microbiota Transplantation (FMT): Modifying the microbiome via transplantation as last resort is being investigated to reverse dysbiosis. Disclaimer: While study in mice and early human trial show promise, therapeutic intervention targeting the microbiome for Alzheimer's are still under investigation don't drink sugar nor eat a high carb diet be on a low carb diet & drink cement heavy water hard water not sugar nor beer Supplement with the 7 Kosher supplements of Methuselah so as to live long avoid gene disorder which mean drink charcoal as a carbon source along yor Hydrogen water Bottle the brain is mostly made of Hydrogen & Carbon the building blocks of Omega 3 fatty acids & supplement with Arginine for Nitrogen production all neurotransmitters are partly made of Nitrogen also Phosphorus supplement & Oxygen along with 72 Trace Minerals of Natures plus these precious health biohackers replenish gray & white matter of the brain which naturaly shrink with age due to lack of fatty acids & building blocks of life Carbon Hydrogen Nitrogen Oxygen & Phosphorus take Kilograms of Silica as gravel gastroliths for orthosilicic acid production take care of your health your diet cannot consist of protein sugar & carbs alone you need dietary supplement the human body is not only made of meat & salad don't forget about MSM 30% SUlfur just remember Sulfur is a mineral present main ingredient in top Alzheimer medicine be blessed by God the Father God the Son & God the Holy Spirit Hallelujah Hallelujah Blessed be the word of the Lord for Christ is risen Hallelujah Hallelujah peace be still in Nomine Patris et FiLii et Spiritus Sancti amen
https://www.youtube.com/watch?v=zTd0-A5yDZI
Inside Alzheimer’s disease
https://www.youtube.com/watch?v=YMwZIqWQl-k
Alzheimer's Disease: Latest Research and Prevention Strategies
https://www.youtube.com/watch?v=IG_iwNY3woI
Transmission of misfolded proteins in neurodegenerative disorders (Dr. Virginia Lee}
https://www.youtube.com/watch?v=BW2zN3J2lfs
ALZHEIMER'S - CAN WE PREVENT IT?
https://www.youtube.com/watch?v=k_P7Y0-wgos
The Man With The Seven Second Memory
https://www.youtube.com/watch?v=RmGqfOxgKXw
Alzheimer's Disease: A Beautiful Mind is a Horrible Thing to Waste
https://www.youtube.com/watch?v=8wAwQ6F7yWA
'Miracle' drug giving hope to Alzheimer's sufferers | 60 Minutes Australia
https://www.youtube.com/watch?v=Ow217dYc3Uw
New Alzheimer's drug approved in Australia | 7NEWS
https://www.youtube.com/watch?v=dS_cJferURA
How a Medical Mystery in Guam Led to a New Approach to Alzheimer’s Disease
https://www.youtube.com/watch?v=oXKnc3OlTXo
Alzheimer's Disease - Pathology, Tangles, Beta Amyloids
https://www.youtube.com/watch?v=bQsgiBh0QCY
Mechanism of Alzheimer's Disease
https://www.youtube.com/watch?v=cJGTLgkxST8
Can Alzheimer's Be Prevented? The Neuroscience of Aging and Memory Loss
https://www.youtube.com/watch?v=V1NziI4Iyf4
Scientists Are So Close to Curing Alzheimer's. Here's Why
https://www.youtube.com/watch?v=fJobcypPZpM
How new Alzheimer's drug Leqembi works, risks and who might benefit
https://www.youtube.com/watch?v=3xI9c-PkIFg
US approves first new Alzheimer's drug in 20 years - BBC News
https://www.youtube.com/watch?v=3UmC3fenCcY
The race to find a treatment for dementia | Four Corners
