Firas Ghanem
Beirut, Lebanon
Nancy Chedid
Cambridge, Massachusetts, United States

“On my good days, I can almost pass for a normal person, and on my bad days, I feel like I can’t find myself. I’ve always been so defined by my intellect, my language, my articulation, and now sometimes I can see the words hanging in front of me, and I can’t reach them, and I don’t know who I am, and I don’t know what I’m going to lose next.”¹

In her debut novel Still Alice and its subsequent movie adaptation, author and neuroscientist Lisa Genova depicts the fictional Alice Howland, a distinguished linguistics professor celebrated for her intellectual acumen. However, Howland’s brilliant life takes a solemn turn on her 50^th birthday when a genetic test delivers the grim diagnosis of early-onset Alzheimer’s disease, a variant typically affecting 5–10% of those with the disease.² This rare familial form of Alzheimer’s can strike individuals as young as 28.³

Despite several genetic clues, the etiology of Alzheimer’s remains elusive. Events in the brain include beta-amyloid peptides accumulating extracellularly, disrupting normal brain function. Mutations in the PSEN1 or PSEN2 genes exacerbate neurotoxic beta-amyloid production. In addition, the tau protein, typically involved in microtubule stability, undergoes excessive chemical changes and triggers abnormal helical aggregations within neurons, forming distinctive neurofibrillary tangles. Cortical atrophy, widened cerebral sulci, and compensatory ventricular enlargement follow. Microscopic pathologic changes (neurofibrillary tangles and beta-amyloid neuritic plaques) in the hippocampus, a region critical for memory, underline Alzheimer’s severity.⁴ Importantly, Alzheimer’s often coexists with other forms of dementia such as cerebrovascular disease and Lewy body disease, complicating diagnosis and management.

Clinically, Alzheimer’s disease presents as the gradual onset and steady progression of memory impairment. It first affects episodic memory (recollections of specific events) but later extends to knowledge of facts, vocabulary, and concepts. The decline further impairs executive function and judgment, impacting daily tasks and self-awareness. Early visuospatial impairments are followed by language deficits (aphasia) and impaired mobility (apraxia, shuffling gait with muscle rigidity, awkward movement, etc.). Symptoms like sleep disturbances, apathy, irritability, and later-stage possible agitation, aggression, and psychosis pose significant challenges for caregivers.

Lisa Genova’s tale raises profound ethical and existential questions about the essence of human identity. Alzheimer’s and related dementia disorders disrupt not only memory but also the essence of self, causing individuals to lose their grip on their past, present, and future selves. Consequently, the question of “Who am I?” becomes increasingly elusive for those dealing with dementia.

In the philosophical arena, two predominant paradigms govern the understanding of personal identity. The first, rooted in individualism and tracing its origins to René Descartes and John Locke, posits that memory and identity are inextricably entwined. Descartes’ famous maxim, “I think, therefore I am,” emphasizes the inner workings of the self as the bedrock of reality and memory as a testament to existence. Public discussions about dementia often fall within this memory-centric paradigm, emphasizing the preservation of memory and cognitive faculties. External aids such as sticky notes, and ambitious technologies such as brain implants, offer important support for maintaining daily memory function. An alternative perspective, advocated by Martin Heidegger and Maurice Merleau-Ponty, challenges the notion of a self confined within the recesses of one’s mind. According to this perspective, identity arises through interactions shaped by shared language, culture, and mutual recognition. Individuals are not solitary entities but rather intricate constellations of roles (spouses, parents, friends, colleagues, etc.), each contributing to the narrative of selfhood. Dementia disrupts these shared presuppositions, straining the bonds that underpin communication and identity.

From either perspective, creating supportive environments that accommodate individuals with dementia becomes paramount. Simplified, well-lit surroundings with minimal cognitive demands are favored, allowing for repetitive actions that ground one’s sense of self. As memory recedes, emotions, feelings, and physical experiences come to the forefront, offering alternative pathways for redefining the self. This shift potentially offers more meaningful and compassionate care while enriching one’s understanding of what it means to be human. Instead of imposing systems ill-suited for individuals confronting dementia, society should endorse more compassionate and less judgmental methodologies. It is a collective responsibility to relinquish temptations to discard those whose memories fail and to instead share in this human voyage, wherein empathy transcends judgement.

Amid the erosion of memory, Alice Howland discovers that her identity extends beyond her fading memories. She uncovers the elixir of being, where recollections may dim, but the radiance of the present shines undiminished. This enduring vitality thrives in shared moments, the embrace of loved ones, and the pure joy of the present. As Alice eloquently articulates in her address to the US Alzheimer’s Society:

For the time being, I’m still alive. I know I’m alive. I have people I love dearly. I have things I want to do with my life. I rail against myself for not being able to remember things, but I still have moments in the day of pure happiness and joy. And please do not think that I am suffering. I am not suffering. I am struggling. Struggling to be part of things, to stay connected to who I once was. So, “live in the moment,” I tell myself. It’s really all I can do, live in the moment.¹

References

1. Still Alice. Directed by Richard Glatzer and Wash Westmoreland. Los Angeles, CA: Sony Pictures Classics; 2014.
2. Reitz C, Rogaeva E, Beecham GW. Late-onset vs nonmendelian early-onset Alzheimer disease: A distinction without a difference?. Neurol Genet. 2020;6(5):e512. doi:10.1212/NXG.0000000000000512
3. Alzheimer’s Association. Alzheimer’s disease facts and figure. 2025. https://www.alz.org/media/Documents/alzheimers-facts-and-figures.pdf
4. Lakhan SE. Alzheimer’s Disease. Medscape. 2021. https://emedicine.medscape.com/article/1134817